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Archive for May, 2008

Circumcision Gains Ground As AIDS Weapon In Kenya

Posted by pozlife on May 27, 2008

by The Associated Press

Posted: May 26, 2008 – 8:00 am ET

(Kisumu, Kenya) Sitting underneath the bright murals at a clinic, 22-year-old Elijah Ochanda gestures at his shorts and explains: “When they remove this thing, it makes you safer.”

He is talking about the circumcision he is about to undergo at the urging of his older brother. He has watched several friends die of AIDS, and has come to believe the science that says circumcision can prevent men from being infected.

Dr. Robert Bailey, an epidemiology professor from the University of Illinois, is helping to roll out Kenya’s first free circumcision project, which offers operations at public health facilities. Such projects are already running in Swaziland, Rwanda and Zambia, other countries where a large percentage of the population traditionally do not circumcise.

Bailey’s study in Kisumu, western Kenya found infection rates were cut by 60 per cent among men who were circumcised. The study, funded by the U.S. Institutes of Health and the Canadian Institutes of Health Research, was one of several that led the World Health Organization to include circumcision in its prevention policies a year ago.

It prompted the Kenyan government to form a task force to promote voluntary, medically safe operations.

But it’s not that simple. Circumcision has become entangled in the violence that followed the disputed presidential election last December.

Supporters of President Mwai Kibaki, whose Kikuyu tribe circumcises its men, clashed with supporters of opposition leader Raila Odinga, who is Luo, a tribe that does not circumcise. The rite took on political significance, with Odinga’s rivals publicly saying he wasn’t a complete man. Many Luo were forcibly circumcised in the violence.

The violence has subsided, but Bailey says it has made the new power-sharing government, with Odinga as prime minister, wary of taking a public stance on circumcision. The disruption initially delayed the launch of the task force’s program.

Still, it’s noteworthy that Ochanda has overcome the tradition issue in opting for circumcision. And the Luo tribe’s council of elders doesn’t forbid it outright although they do say it is contrary to their traditions and worry it will promote promiscuity.

“If you want to do that on your own, no one will question you, but it is not our custom,” said elder Odungi Randa.


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Despite H.I.V., Fighting to Maintain Health and a Positive Attitude

Posted by pozlife on May 27, 2008


Nicole Bengiveno/The New York Times

Frances Melendez, left, who leads the Divas, a support group for H.I.V.-positive women in Harlem, with a client, Patricia Clouden.


Published: May 18, 2008

Patricia Clouden dresses in a whirl of color, from her bright African dress to her shiny green toenail polish. She is a grandmother of eight who gets noticed in her Harlem neighborhood and is not afraid to speak her mind.

“I’m not a ‘Yes, ma’am’ no more,” she told a group of about a dozen women seated around a boardroom table one recent afternoon. “I’m a warrior.”

Ms. Clouden was not speaking at a corporate team-building event but at a meeting of the Divas, a support group made up of African-American and Hispanic women over 50 who are H.I.V. positive. Many of these women contracted the virus from unfaithful partners, or from lacking the self-esteem to demand safe sex. The Divas, one of many support groups organized through Iris House, an AIDS service center in Harlem, is, more than anything, about rebuilding that self-esteem.

“H.I.V. saved my life,” said Ms. Clouden, who is 59 and received a diagnosis of H.I.V. after becoming ill in 2003, at the end of an abusive 20-year relationship. Her bright clothing is a kind of camouflage; her withered, blinded right eye is a permanent reminder of the violence she endured. Given her history, once she contracted H.I.V., Ms. Clouden said, “I didn’t expect I would see grandchildren.”

She and the other Divas represent the changing face of H.I.V. and AIDS: The Centers for Disease Control and Prevention reported that in 2005, 27 percent of people with AIDS were women, up from less than 5 percent two decades before, and that African-American women were 23 times more likely than white women to become infected. AIDS is the fourth-leading cause of death for black women older than 45 and Hispanic women aged 35 to 44, according to the C.D.C.; blacks and Hispanics make up 24 percent of the nation’s female population, but 82 percent of new AIDS diagnoses among women.

And the neighborhoods around Iris House have some of the highest infection rates in the country. In Harlem, 116 of every 100,000 people are H.I.V.-positive, compared with 46 per 100,000 in New York City and 18.5 in the nation.

“We like to call Central Harlem, East Harlem and the South Bronx ground zero,” said Ingrid Floyd, executive director of Iris House.

Noting that many of the clients she sees are poor and have experienced homelessness, domestic violence and drug addiction, Ms. Floyd said that low self-esteem continues to put obstacles in their path.

“They are not as empowered, not as educated as their Caucasian counterparts and hence they are being hit most with H.I.V.,” she said. “A lot of times we have clients who have gone into depression, and they isolate themselves. So, they stay in their apartments and they don’t come out, because they think they are going to die.”

Iris House, named for Iris de la Cruz, who died of AIDS in 1991 after working as an advocate for women with the disease, opened 15 years ago as one of the first women-centered AIDS groups in the nation. Financed by foundations and individuals, the organization distributes 100,000 condoms a month on neighborhood streets and provides counseling and cooking classes to people with H.I.V. and AIDS.

The Divas, one of half a dozen specialty groups that meet at Iris House, have discussions on Wednesdays about sexuality and sensuality, medication and mental health. Its members also take exercise classes and attend workshops on managing their finances. The oldest member is 76, the youngest 50. The name comes from a nickname for Frances Melendez, a psychologist who runs the group and acts the part.

Many of the Divas said that the group has helped them talk openly and honestly about sex for the first time in their lives. They not only look back on how they were infected, but also discuss expectations for future relationships.

At one recent group session, some of the women said they had been so burned by their past partners that they were now more interested in companionship than in sex.

“We need someone to hold us,” said one of the Divas, who learned that she was H.I.V. positive in 1995, a week before her companion died of AIDS, and spoke on the condition she not be named. “Sex is something we grew into and grew out of.”

Dr. Melendez gently guided the discussion, asking whether the women felt comfortable looking at themselves naked, noting that H.I.V. and age have done their damage. Some shook their heads, but one woman announced: “I love hugging myself.”

There was a pause, and then another leaned forward: “I’m a mirror person.”

Instead of nervous laughter, the women encouraged one another with a chorus of “Amen” and “Go ahead, baby.”

Dr. Melendez said that the aim of the group was to arm the women with renewed life-management skills and the strength and confidence to live beyond the initial shock and despair of the diagnosis. For some, learning of their H.I.V. status was such a shock that they have used it as a way to restart their lives.

“It is a very difficult decision to decide to live positively,” Dr. Melendez said. “It’s much easier to say ‘forget it’ and let the disease take its course.”

Kathy, 56, a plainly dressed woman with neat hair who spoke on the condition that her last name not be used, has been fighting her own battle against H.I.V. since she received the diagnosis in 1992.

“I didn’t expect to see my children or go to a wedding,” Kathy said in an interview after the group session. “They gave me a death sentence. But, 16 years later, I’m still here.”

She said she suspected that she contracted H.I.V. from her partner; she thought he was unfaithful to her, but felt it was her duty to stay with him. She attributes her longevity to vigilance about her diet and medication regimen.

But her voice still breaks and she shudders when she dares to speak of a long life ahead. “My future is very bright,” she said, her words betrayed by her tentative tone. “I’m going to see my grandchildren graduate.”

The woman who learned of her H.I.V. in 1995 said that when she told her six children about her illness, “they all hugged me and caressed me, and it has been like that ever since.”

But she is reluctant to disclose her H.I.V. status beyond her family, and sees the virus almost as a parasite that she is determined to keep under control. “I got a squatter in the corner, sitting there,” she said after the session. “I tell him he’s living in my temple and he has to do as I say to do.”

Ms. Clouden said that when she first tested positive for H.I.V., after becoming breathless while walking home up a hill five years ago, she thought to herself, “Oh, Lord, I guess I’m going to die.”

She said that she mostly stayed at home to raise her four children, but that she worked occasionally as a nurse’s aide and a hotel maid, in part for the money and in part as an escape from her violent companion. The worst of his attacks, she said, came as retribution for her walking past him without noticing that he was there.

“He beat me up, and he took his finger and stuck it in my eye and pulled my eye out,” she recalled, adding that she did not go to a hospital for fear of getting him in trouble. “I felt that I wasn’t good enough, that I was ugly. I felt that I needed somebody to love me.

“My mother already had a plot with my name on it,” she added. “So at least she would have someplace to bury me.”

Several of the Divas said that they had not disclosed their H.I.V. status to their friends and family, so the group provides a rare safe haven. “I’m hoping they don’t see the diagnosis as loneliness,” Dr. Melendez said.

Ms. Floyd said that women who were infected with H.I.V. still did not receive the same support and empathy as those diagnosed with other illnesses, like cancer.

“When a woman comes out and says she has breast cancer, everybody rallies around her,” she said. “I live for the day when someone saying they have an H.I.V. diagnosis is the same as someone saying they have breast cancer.”

For Ms. Clouden, the Divas have made it that way. “We used to cower behind our insecurities,” she said, speaking as much for herself as for the others in the group. “But, now our insecurities are cowering behind us, because we are the Divas.”

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Web Game With a Message Debunks H.I.V. Myths

Posted by pozlife on May 27, 2008


Published: May 19, 2008

Hot or Not, a Web site where people submit photographs of themselves so that strangers can rate how attractive they are on a scale of 1 to 10, has spawned many imitators (plus a fair number of critics who view it as a sign of the end of civilization as we know it).

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Times Health Guide: H.I.V. Infection

One new spinoff, Pos or Not, has a serious purpose (tasteful or not). The site, www.posornot.com, introduced in late April, is an H.I.V. education effort disguised as a game. It shows photographs and brief biographies of men and women ages 21 to 30, and asks visitors to decide whether each is H.I.V. positive or negative. The message is that you can’t judge someone’s virus status by looks, occupation or taste in music.

The site is sponsored by MTV’s college network and the Kaiser Family Foundation, a nonprofit group that focuses on health policy. “We feel it’s another kind of activist tool to get out the word about H.I.V. protection,” said Stephen K. Friedman, the general manager of mtvU, the college and university offshoot of Viacom’s MTV network.

The first trial by mtvU of what Mr. Friedman calls “games for change” was Darfur Is Dying, an online simulation of a refugee camp that has logged more than 1.5 million plays since 2006. Other companies have sponsored games about the Israeli-Palestinian conflict, the immigration debate and the world’s water resources.

The network wants the word about its H.I.V. site and its message to be spread like a popular YouTube video. It enlisted celebrities like Wyclef Jean, a musician, and Rosario Dawson, an actress, to make promotions for the game, which are playing across MTV’s networks.

The game — if it can really be called that — was played about 5.1 million times by 400,000 people in its first three weeks, according to mtvU. Entertainment Weekly’s Web site suggested it might be the “most depressing use” of an Internet trend ever, but suggested that any H.I.V. outreach effort could be beneficial.

Mr. Friedman said that in a media-saturated climate, maybe young people have to be shocked into paying attention. “Looking at the statistics that one in four people who are H.I.V. positive in the U.S. don’t know it, it’s pretty staggering,” he said. “We hope that something like this will get under their skin.”

“If it makes some people uncomfortable,” he added, “that’s not necessarily a bad thing.”

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Prison for Man With H.I.V. Who Spit on a Police Officer

Posted by pozlife on May 27, 2008


Published: May 16, 2008

DALLAS — A homeless man who spit in the mouth and eye of a police officer and then taunted him, saying he was H.I.V. positive, was sentenced to 35 years in prison on Wednesday for harassing a public servant with a deadly weapon: his saliva.

Because of the deadly weapon finding, the man, Willie Campbell, 42, of Dallas, will not be eligible for parole until he has served half his sentence.

In May 2006, a passer-by reported an unconscious man, Mr. Campbell, sprawled outside a downtown Dallas building. Mr. Campbell tried to fight paramedics and kicked the police officer who arrested him for public intoxication, prosecutors said.

The police reported that Mr. Campbell spat at an officer and said he had H.I.V., the virus that causes AIDS, as they struggled to move him to a squad car.

During the trial, Mr. Campbell, who prosecutors say has been H.I.V. positive since 1994, denied that he had resisted arrest or spit at an officer, his lawyer, Russell Henrichs, said Thursday.

Mr. Henrichs added that his client had been indicted under a habitual-offender statute that increased the penalty in his case to a minimum of 25 years in prison, because he had been convicted of attacking two other officers in a similar manner and biting two inmates, as well as more than two dozen other offenses.

“You can see why we thought that we needed to get this guy off the streets,” said Jenni Morse, who prosecuted the current case.

None of the three officers attacked by Mr. Campbell contracted H.I.V., Ms. Morse said.

After Mr. Campbell was convicted by a jury, he shouted at the prosecutor and police officers, calling them liars and telling them to “rot in hell” for “railroading an innocent man.” He was forced to listen to the rest of sentencing from a holding cell.

Mr. Campbell waived his right to appeal and is awaiting transfer from the Dallas jail to prison.

According to the Centers for Disease Control and Prevention, H.I.V. is primarily spread through sexual contact or the exchange of blood. Although there have been rare cases of transmission through severe bites, “contact with saliva, tears or sweat has never been shown to result in transmission of H.I.V.,” the agency reports.

Lambda Legal, which advocates for people living with the virus, says saliva should not be considered a deadly weapon.

“There’s still an incredible amount of ignorance about H.I.V. and how H.I.V. is or isn’t transmitted,” said Bebe Anderson, the organization’s H.I.V. project director. “It’s regrettable.”

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Gay, Punk and Ever the Provocateur

Posted by pozlife on May 27, 2008


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Published: May 25, 2008

WITH each passing year the British artist and iconoclast Derek Jarman seems at once more important and more marginal. His place in history as a pioneering gay filmmaker is secure, but his work remains little seen, and the spirit in which it was made seems further away than ever.

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Leon Morris/Getty Images

Politics and aesthetics were inseparable in the films of Derek Jarman.


Filmography: Derek Jarman

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Zeitgeist Films

Derek Jarman’s film “Caravaggio” (1986), with Dexter Fletcher.

Mr. Jarman died of complications from AIDS in 1994, at 52, and perhaps the time is ripe for reappraisal. “Derek,” a documentary tribute by Isaac Julien that had its premiere at the Sundance Film Festival in January, will screen at the Museum of Modern Art in New York from June 9 through 16. On June 24 Zeitgeist Films, the distributor that helped introduce Mr. Jarman to American audiences, is releasing “Glitterbox,” a DVD set that represents a cross section of his films: the neo-Brechtian biopics “Caravaggio” (1986) and “Wittgenstein” (1993); the homoerotic reverie “The Angelic Conversation” (1985); and his monochrome valediction, “Blue” (1993), as moving an epitaph as any artist has ever composed for himself.

Mr. Julien’s “Derek” combines clips from Mr. Jarman’s movies, excerpts from a 1990 interview and a ruminative voice-over by Tilda Swinton, who also served as executive producer. In an e-mail message, Ms. Swinton, a frequent collaborator of Mr. Jarman’s whose first film role was in “Caravaggio,” said the documentary had been prompted in part by the blank looks she received when talking about him to aspiring filmmakers.

“It feels like the correct time to be reminded of an ancient tradition that has always served civilization well,” she said, “that of the independent, truth-telling poet provocateur.”

Mr. Jarman himself, despite his tendency toward rebellion, drew heavily on the example of previous generations. His poetic sensibility owes a debt to the outlaw lyricism of Jean Cocteau and Jean Genet. His taste for the baroque calls to mind British filmmakers like Michael Powell and Ken Russell (who hired him as a set designer). There are also kinships with the bad-boy iconoclasts he memorialized: Caravaggio, the painter who revolted against the refinement of the Renaissance, and Ludwig Wittgenstein, the philosopher who regarded the academy with hostility.

Mr. Jarman once lamented that heterosexuals had so colonized and despoiled the screen — his actual phrasing was less polite — “that there’s hardly room for us to kiss.” He made it his mission to create that room. His first feature, “Sebastiane” (1976), an ancient Roman idyll that made explicit the gay subtext of the sword-and-sandal epic, was not just candid but also celebratory in depicting homosexual desire. It sparked some condemnation but was among the first films showing an erection to make it past the British censors.

Despite the dandyish elements of Mr. Jarman’s work, he was at heart a punk filmmaker — a connection reinforced by “Jubilee” (1977), which dramatizes punk’s “no future” nihilism with the help of a time-traveling Queen Elizabeth I. Mr. Jarman called himself a “controversialist,” but he was no mere troublemaker. Aesthetics and politics were, for him, inseparable. His signature combination of beauty, wit and anger was a polemical stance.

His filmmaking career coincided with the reign of Margaret Thatcher, an archnemesis and a kind of negative muse. In public and in films like “The Last of England” (1988), he railed against what he saw as the ruinous greed and soullessness of Britain in the ’80s. Thatcher-era policies scaled back government support of the film industry, but inhospitable conditions only seemed to bolster his do-it-yourself resourcefulness and sense of artistic community.

Trained as a painter, Mr. Jarman appreciated the communal aspect of filmmaking. “I think he made films primarily for the company,” Ms. Swinton said. “Working with him was to work alongside him.”

Mr. Jarman’s life fed his art, and vice versa. It was not a surprise that his impending death became central to his work. Fighting the stigma of AIDS just as he fought the stigma of being gay, he spoke openly about his H.I.V.-positive status. The films that followed the diagnosis of his disease, especially “The Last of England” and his anachronistic Christopher Marlowe adaptation, “Edward II” (1991), are notable for their fury and lucidity.

By the time he made “Wittgenstein,” not long before his death, his eyesight was failing — hence the boldly exaggerated color scheme. His final feature, “Blue,” which for 76 minutes pairs an aural collage with a solid screen of deep blue (the shade patented by the painter Yves Klein), seeks both to represent and to transcend his blindness and the abyss of mortality.

Today Mr. Jarman is considered the founding father of what came to be known as the New Queer Cinema, a loose grouping of filmmakers — among them Todd Haynes (“Poison”), Tom Kalin (“Swoon”) and Mr. Julien (“Looking for Langston”) — who emerged in the late ’80s. But as Mr. Julien said in an e-mail message, “Derek paved the way for independent filmmakers, period — not just queer filmmakers.” Of particular relevance, he added, was the way Mr. Jarman “prophetically refused to be tied to a single medium,” insisting on a continuity among his works in film, installation, painting, sculpture, design and poetry.

Mr. Jarman in some ways seems well remembered in his native country. The Film London agency recently established the Jarman Award for young filmmakers. The garden he tended at his cottage on the English coast has become a tourist attraction. But as “Derek” suggests — with scenes of Ms. Swinton wandering around pristine present-day London, as if looking for traces of him — much of what he stood for has vanished. In other words, it is hard to imagine an oppositional artist like Mr. Jarman emerging, let alone thriving, in the current climate.

Mr. Jarman took pride in remaining outside the British film establishment, in never being marketable enough to count as an official export. With that in mind, how does Ms. Swinton think he would have reacted to her recent Oscar win for “Michael Clayton”?

“I think he would have laughed and laughed and laughed and laughed and laughed,” she said in her e-mail message. “And then,” she added, referring to her golden statuette, “he would ask me for the thing to melt it down into an artwork.”

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Scientists Find New Receptor for H.I.V. – New York Times

Posted by pozlife on May 27, 2008


Published: February 11, 2008

SAN FRANCISCO — Government scientists have discovered a new way that H.I.V. attacks human cells, an advance that could provide fresh avenues for the development of additional therapies to stop AIDS, they reported on Sunday.


Health Guide: AIDS

The discovery is the identification of a new human receptor for H.I.V. The receptor helps guide the virus to the gut after it gains entry to the body, where it begins its relentless attack on the immune system.

The findings were reported online Sunday in the journal Nature Immunology by a team headed by Dr. Anthony S. Fauci, the director of the National Institute of Allergy and Infectious Diseases.

For years, scientists have known that H.I.V. rapidly invades the lymph nodes and lymph tissues that are abundant throughout the gut, or intestines. The gut becomes the prime site for replication of H.I.V., and the virus then goes on to deplete the lymph tissue of the key CD4 H.I.V.-fighting immune cells.

That situation occurs in all H.I.V.-infected individuals, whether they acquired the virus through sexual intercourse, blood transfusions, blood contamination of needles and syringes, or in passage through the birth canal or drinking breast milk.

The findings appear to provide some, if not the main, answers to how and why that situation occurs.

Dr. Warner C. Greene, an AIDS expert and the director of the Gladstone Institute of Virology and Immunology here who was not involved in the research, said the findings were “an important advance in the field.”

“They begin to shed light on the mysterious process on why the virus preferentially grows in the gut,” Dr. Greene said in an interview.

Dr. Fauci, James Arthos, Claudia Cicala, Elena Martinelli and their colleagues showed that a molecule, integrin alpha-4 beta-7, which naturally directs immune cells to the gut, is also a receptor for H.I.V. A protein on the virus’s envelope, or outer shell, sticks to a molecule in the receptor that is linked specifically to the way CD4 cells home in on the gut, the researchers said.

Binding of the virus to the integrin alpha-4 beta 7 molecule stimulates activation of another molecule, LFA-1, which plays a crucial role in the spread of the virus from one cell to another. The actions ultimately lead to destruction of lymph tissue, particularly in the gut.

Several other receptor sites for H.I.V. are known. The most important is the CD4 molecule on certain immune cells; the molecule’s role as an H.I.V. receptor was identified in 1984.

Two other important receptors, known as CCR5 and CXCR4, were identified in 1996. CCR5 is a normal component of human cells and acts as a doorway for the entry of H.I.V. People who lack it because of a genetic mutation rarely become infected even if they have been exposed to H.I.V. repeatedly.

“The work we did took nearly two years, and there’s little doubt that what we have found is a new receptor,” Dr. Fauci said in an interview after giving a lecture here, adding that “we certainly have to learn a lot more about it.”

Scientists have sought to identify receptors because they offer targets for the development of new classes of drugs.

For example, last year the Food and Drug Administration approved for AIDS treatment a Pfizer drug, Selzentry or maraviroc, which works by blocking CCR5.

Dr. Fauci said he hoped his team’s findings would encourage other scientists from different disciplines to explore new ways to attack H.I.V.

A number of experimental drugs that block the integrin alpha-4 beta-7 receptor are being tested for the treatment of autoimmune disorders. Dr. Fauci said such drugs should also be studied for their potential benefit in AIDS treatment.

Organization of new trials in the next year or so could test such drugs in animals and humans to determine their safety and effectiveness against H.I.V., Dr. Fauci said.

One candidate is a drug, Tysabri or natalizumab, that is marketed for treatment of multiple sclerosis, Dr. Fauci said. Biogen/Elan makes Tysabri.

If trials for H.I.V. are successful, Dr. Fauci said, the drugs could be added to existing treatment regimens.

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HIV/AIDS: Signs and symptoms – MayoClinic.com

Posted by pozlife on May 26, 2008


Signs and symptoms

The symptoms of HIV and AIDS vary, depending on the phase of infection. When first infected with HIV, you may have no symptoms at all, although it’s more common to develop a brief flu-like illness two to six weeks after becoming infected. But because the signs and symptoms of an initial infection — which may include fever, headache, sore throat, swollen lymph glands and rash — are similar to those of other diseases, you might not realize you’ve been infected with HIV.

Even if you don’t have symptoms, you’re still able to transmit the virus to others. Once the virus enters your body, your own immune system also comes under attack. The virus multiplies in your lymph nodes and slowly begins to destroy your helper T cells (CD4 lymphocytes) — the white blood cells that coordinate your entire immune system.

You may remain symptom-free for eight or nine years or more. But as the virus continues to multiply and destroy immune cells, you may develop mild infections or chronic symptoms such as:

  • Swollen lymph nodes — often one of the first signs of HIV infection
  • Diarrhea
  • Weight loss
  • Fever
  • Cough and shortness of breath

During the last phase of HIV — which occurs approximately 10 or more years after the initial infection — more serious symptoms may begin to appear, and the infection may then meet the official definition of AIDS. In 1993, the Centers for Disease Control and Prevention (CDC) redefined AIDS to mean the presence of HIV infection as shown by a positive HIV-antibody test plus at least one of the following:

  • The development of an opportunistic infection — an infection that occurs when your immune system is impaired — such as Pneumocystis carinii pneumonia (PCP)
  • A CD4 lymphocyte count of 200 or less — a normal count ranges from 600 to 1,000

By the time AIDS develops, your immune system has been severely damaged, making you susceptible to opportunistic infections. The signs and symptoms of some of these infections may include:

  • Soaking night sweats
  • Shaking chills or fever higher than 100 F for several weeks
  • Dry cough and shortness of breath
  • Chronic diarrhea
  • Persistent white spots or unusual lesions on your tongue or in your mouth
  • Headaches
  • Blurred and distorted vision
  • Weight loss

You may also begin to experience signs and symptoms of later stage HIV infection itself, such as:

  • Persistent, unexplained fatigue
  • Soaking night sweats
  • Shaking chills or fever higher than 100 F for several weeks
  • Swelling of lymph nodes for more than three months
  • Chronic diarrhea
  • Persistent headaches

If you’re infected with HIV, you’re also more likely to develop certain cancers, especially Kaposi’s sarcoma, cervical cancer and lymphoma, although improved treatments have reduced the risk of these illnesses.

Symptoms of HIV in children
Children who are HIV-positive often fail to gain weight or grow normally. As the disease progresses, they may have difficulty walking or delayed mental development. In addition to being susceptible to the same opportunistic infections that adults are, children may have severe forms of common childhood illnesses such as ear infections (otitis media), pneumonia and tonsillitis.


Normally, white blood cells and antibodies attack and destroy foreign organisms that enter your body. This response is coordinated by white blood cells known as CD4 lymphocytes. These lymphocytes are also the main targets of HIV, which attaches to the cells and then enters them. Once inside, the virus inserts its own genetic material into the lymphocytes and uses them to make copies of itself.

When the new copies of the virus break out of the host cells and enter the bloodstream, they search for other cells to attack. In the meantime, the old host cells and some uninfected CD4 cells die from the effects of the virus. The cycle repeats itself again and again. In the process, billions of new HIV particles are produced every day. Eventually, the number of CD4 cells in the body decreases, leading to severe immune deficiency, which means your body can no longer effectively fight off viruses and bacteria that cause disease.

How HIV is transmitted
You can become infected with HIV in several ways, including:

  • Sexual transmission. You may become infected if you have vaginal, anal or oral sex with an infected partner whose blood, semen or vaginal secretions enter your body. You can also become infected from shared sexual devices if they’re not washed or covered with a condom. The virus is present in the semen or vaginal secretions of someone who’s infected and enters your body through small tears that can develop in the rectum or vagina during sexual activity. If you already have another sexually transmitted disease, you’re at much greater risk of contracting HIV. Contrary to what researchers once believed, women who use the spermicide nonoxynol-9 also may be at increased risk. This spermicide irritates the lining of the vagina and may cause tears that allow the virus into the body.
  • Transmission through infected blood. In some cases, the virus may be transmitted through blood and blood products that you receive in blood transfusions. This includes whole blood, packed red cells, fresh-frozen plasma and platelets. In 1985, American hospitals and blood banks began screening the blood supply for HIV antibodies. This blood testing, along with improvements in donor screening and recruitment practices, has substantially reduced the risk of acquiring HIV through a transfusion.
  • Transmission through needle sharing. HIV is easily transmitted through needles and syringes contaminated with infected blood. Sharing intravenous drug paraphernalia puts you at high risk of HIV and other infectious diseases such as hepatitis. Your risk is greater if you inject drugs frequently or also engage in high-risk sexual behavior. Avoiding the use of injected drugs is the most reliable way to prevent infection. If that isn’t an option, you can reduce your risk by sterilizing injection paraphernalia with household bleach or by participating in a needle exchange program that allows you to trade used needles and syringes for sterile ones.
  • Transmission through accidental needle sticks. Transmission of the virus between HIV-positive people and health care workers through needle sticks is low. Experts put the risk at far less than 1 percent.
  • Transmission from mother to child. Each year, nearly 600,000 infants are infected with HIV, either during pregnancy or delivery or through breast-feeding. The rate of mother-to-child transmission in resource-poor countries is as much as 40 percent higher than it is in the developed world. But if women receive treatment for HIV infection during pregnancy, the risk to their babies is significantly reduced. Combinations of HIV drugs may reduce the risk of mother-to-child transmission even more. In the United States, most pregnant women are pre-screened for HIV, and anti-retroviral drugs are readily available. Not so in developing nations, where women seldom know their HIV status, and treatment is often limited or nonexistent. When medications aren’t available, Caesarean section is sometimes recommended instead of vaginal delivery, but this isn’t a good option for women in resource-poor countries, where it poses additional risks for both mother and child. Other options, such as vaginal disinfection, haven’t proved effective.
  • Other methods of transmission. In rare cases, the virus may be transmitted through organ or tissue transplants or unsterilized dental or surgical equipment.

Ways HIV is not transmitted
To become infected with HIV, infected blood, semen or vaginal secretions must enter your body. You can’t become infected through ordinary contact — hugging, dancing or shaking hands — with someone who has HIV or AIDS.

Risk factors

HIV crosses all cultures, national borders and religions. Anyone of any age, race, sex or sexual orientation can be infected, but you’re at greatest risk of HIV/AIDS if you:

  • Have unprotected sex with multiple partners. You’re at risk whether you’re heterosexual, homosexual or bisexual. Unprotected sex means having sex without using a new latex or polyurethane condom every time.
  • Have unprotected sex with someone who is HIV-positive.
  • Have another sexually transmitted disease, such as syphilis, herpes, chlamydia, gonorrhea or bacterial vaginosis.
  • Share needles during intravenous drug use.
  • Have hemophilia and received blood products between 1977 and April 1985 — the date standard testing for HIV began.
  • Received a blood transfusion or blood products before 1985.
  • Have fewer copies of a gene called CCL3L1 that helps fight HIV infection.

Newborns or nursing infants whose mothers tested positive for HIV but did not receive treatment also are at high risk.

When to seek medical advice

If you think you may have been infected with HIV or are at risk of contracting the virus, seek medical counseling as soon as possible. Tests are available that can determine your status. The idea of being tested for HIV infection is frightening for many people, yet a majority of Americans say they would support routine HIV testing for all adults. What’s more, testing itself doesn’t make you HIV-positive or HIV-negative and is important not only for your own health but also to prevent transmission of the virus to others.

You can be tested by your doctor or at a hospital, the public health department, a Planned Parenthood clinic or other public clinics. Many clinics don’t charge for HIV tests. Be sure to choose a place in which you feel comfortable and that offers counseling before and after testing. Don’t let concern about what people may think stop you from being tested. For a referral, or to make an appointment for an HIV test at a Planned Parenthood clinic near you, call 800-230-PLAN, or 800-230-7526. You can also contact your local or state health department.

If you’re pregnant, you may want to get tested even if you think you’re not at risk. If you are HIV-positive, treatment with anti-retroviral drugs during your pregnancy can greatly reduce the chances you’ll pass the infection to your baby. And if you engage in a high-risk behavior such as unprotected sex or sharing needles during intravenous drug use, experts recommend that you get tested for HIV every three to six months.

All states and U.S. territories now report positive HIV and AIDS test results to state public health officials to help track the spread of the disease. Most states use name reporting, but the results are released only to the health department and not to anyone else — including the federal government, employers, insurance companies and family members — without your express permission. In addition, legal provisions ensure the highest degree of confidentiality with regard to name-based HIV data. A few states, including Montana and Oregon, use name-to-code reporting. Don’t let the HIV reporting policy prevent you from seeking testing or treatment. If you are concerned about having your name reported, many states offer anonymous testing centers. If you do test positive and seek treatment, however, you will likely have to provide your name to your doctor.

Screening and diagnosis

HIV is diagnosed by testing your blood or oral mucus for the presence of antibodies to the virus. The CDC encourages voluntary HIV testing as a routine part of medical care for all adolescents and adults ages 13 to 64, in new recommendations issued in September 2006. Although the CDC says that everyone should be tested at least once, yearly testing is recommended only for people at high risk of infection.

Unfortunately, HIV tests aren’t accurate immediately after infection because it takes time for your body to develop these antibodies — usually about 12 weeks. In rare cases, it can take up to six months for an HIV test to become positive.

For years, the only available test for HIV was the enzyme-linked immunosorbent assay (ELISA) test that looked for antibodies to the virus in a sample of your blood. If this test was positive — meaning you had antibodies to HIV — the same test was repeated. If the repeat test was also positive for HIV antibodies, you’d then have another confirming blood test called the Western blot test, which checks for the presence of HIV proteins. The Western blot test was important because you may have non-HIV antibodies that cause a false-positive result on the ELISA test. Combining the two types of tests helped ensure that the results were accurate, and you’d receive a diagnosis of HIV only if all three tests were positive.

The downside is that it can take up to two weeks to get the results of the ELISA and Western blot tests, a period of time that can take an emotional toll and that discouraged many people from returning to get their test results. Now, however, several “rapid” tests can give highly accurate information within as little as 20 minutes.

These tests look for antibodies to the virus using a sample of your blood or fluids collected on a treated pad that’s rubbed on your upper and lower gums. The oral test is almost as sensitive as the blood test and eliminates the need for drawing blood. A positive reaction on a rapid test requires a confirming blood test. And because the tests are relatively new and were originally approved for use only in certified laboratories, they may not be available in all locations.

Home tests
A quick search of the Internet can turn up dozens of “do-it-yourself” HIV tests even though it’s illegal to market most of these tests in the United States. Currently, the Food and Drug Administration (FDA) has approved only one HIV test for home use. The Home Access HIV test, marketed by Home Access Health, is as accurate as a clinical test, and all positive results are automatically retested.

Unlike a home pregnancy test, you don’t perform the test yourself. Instead, you mail in a drop of your blood, then call a toll-free number to receive your results in three to seven business days. This approach ensures your privacy and anonymity — you’re identified only by a code number that comes with your kit. The greatest disadvantage is that you’re not offered the counseling that you typically receive in a clinic or doctor’s office, although you’re given referrals for medical and social services. No matter what type of test you choose, if you test positive for an HIV infection, tell your sexual partner or partners right away so that they can be screened and take steps to protect themselves.

If you receive a diagnosis of HIV/AIDS, your doctor will use a test to help predict the probable progression of your disease. This test measures the amount of virus in your blood (viral load). Studies have shown that people with higher viral loads generally fare more poorly than do those with a lower viral load. Viral load tests are also used to decide when to start and when to change your treatment.



HIV infection weakens your immune system, making you highly susceptible to a large number of bacterial, viral, fungal and parasitic infections. You may also be vulnerable to certain types of cancers. But treatment with anti-retroviral drugs has markedly decreased the number of opportunistic infections and cancers affecting people with HIV. It’s now more likely these infections will occur in people who have not had treatment.

Bacterial infections

  • Bacterial pneumonia. Worldwide, this is one of the most common opportunistic infections occurring in people living with HIV/AIDS. Dozens of types of bacteria can cause bacterial pneumonia, which may develop on its own or after you’ve had an upper respiratory infection such as a cold or the flu.
  • Mycobacterium aviumcomplex (MAC). This infection is caused by a group of bacteria referred to by a single name — MAC. The bacteria normally cause an infection of the respiratory tract. But if you have advanced HIV infection and your CD4 lymphocyte count is less than 50, you’re more likely to develop a systemic infection that can affect almost any internal organ, including your bone marrow, liver or spleen. MAC causes nonspecific symptoms such as fever, night sweats, weight loss, stomach pain and diarrhea.
  • Tuberculosis (TB). In resource-poor nations, TB is the most common opportunistic infection associated with HIV and a leading cause of death among people living with AIDS. Millions of people are currently infected with both HIV and tuberculosis, and many experts consider the two diseases twin epidemics. That’s because HIV/AIDS and TB have a deadly symbiotic relationship, in which each fuels the progress of the other. Having HIV makes you more susceptible to TB and far more likely to progress from dormant to active infection. At the same time, TB increases the rate at which the AIDS virus replicates. What’s more, TB often strikes people with HIV years before other problems associated with HIV develop. One of the first indications of HIV infection may be the sudden onset of TB — often in a site outside the lungs. Currently, someone in the world develops TB every second and 5,000 to 6,000 people die of the disease each day.

    If you’re HIV-positive, you should have a simple skin test for TB early in your medical care. If the test is positive, you’ll also need a chest X-ray and other appropriate tests to make sure you don’t have an active infection. If your TB isn’t active, there are treatments to prevent it from becoming active in the future. TB is more worrisome than many other opportunistic infections because it’s highly contagious. You can get TB when someone with the disease coughs or sneezes near you. The bacteria then spread through your blood and lymph nodes to the rest of your body. TB most often affects the lungs, but people with HIV are more likely to have infection at other sites. Multidrug-resistant tuberculosis (MDR-TB), in which the disease resists treatment with traditional antibiotics, is of particular concern to people with HIV/AIDS. Ultimately, however, TB is of concern to everyone because it can affect even people with healthy immune systems.

  • Salmonellosis. You contract this bacterial infection from contaminated food or water. Symptoms include severe diarrhea, fever, chills, abdominal pain and, occasionally, vomiting. Although anyone exposed to salmonella bacteria can become sick, salmonellosis is far more common in people who are HIV-positive. You can reduce your risk by washing your hands carefully after handling food and animals and by cooking meat and eggs thoroughly.
  • Bacillary angiomatosis. Rarely seen in people not infected with HIV, this infection first appears as purplish to bright red patches on your skin. It often resembles Kaposi’s sarcoma, but it can cause disease in other parts of your body, including your liver and spleen.

Viral infections

  • Cytomegalovirus (CMV). This common herpesvirus is transmitted in body fluids such as saliva, blood, urine, semen and breast milk. More than half the adult population has been infected. But a healthy immune system inactivates the virus, and it remains dormant in your body. If your immune system weakens, the virus resurfaces, causing damage to your eyes, digestive tract, lungs or other organs. Most commonly, CMV causes infection and inflammation of your retina (CMV retinitis). If not treated, CMV retinitis can lead to blindness.
  • Viral hepatitis. Viral hepatitis is a viral infection of the liver. Signs and symptoms include yellowing of your skin and the whites of your eyes (jaundice), fatigue, nausea, abdominal pain, loss of appetite and diarrhea. There are several types of viral hepatitis, but the most common are hepatitis A, B and C. Hepatitis B and C can lead to persistent or chronic infection and put you at risk of long-term complications such as cirrhosis or liver cancer. If you are HIV-positive and also have hepatitis, you may be more likely to develop liver toxicity from your medications.
  • Herpes simplex virus (HSV). HSV, which usually causes genital herpes, may be transmitted during unprotected anal or vaginal sex. Initial symptoms include pain or irritated skin in the genital area. Later, sores that ooze and bleed erupt on the genitals, buttocks and anus. Although these sores eventually heal, the virus periodically reappears, causing the same symptoms. If you have HIV, your skin infection is likely to be more severe than it would be in people who don’t have HIV, and the sores may take longer to heal. Systemic symptoms may also be more severe. Although the herpes virus isn’t life-threatening in adults, it may cause brain damage, blindness or death in infants infected during delivery.
  • Human papillomavirus (HPV). This is one of the most common causes of sexually transmitted disease. Some types of this virus cause common warts; others cause warts on the genitals. If you’re HIV-positive, you’re especially susceptible to infection with HPV and more prone to recurrent infections. HPV infection is especially serious because it significantly increases a woman’s risk of cervical cancer. Infection with both HPV and HIV increases a woman’s risk even further — cervical cancer seems to occur more often and more aggressively in women who are HIV-positive. In 2006, the Food and Drug Administration approved the first vaccine to offer protection from the most dangerous types of HPV. The vaccine is most effective when given to girls before they become sexually active, but it also provides protection for sexually active women age 26 and younger. If you are not a candidate for the vaccine, are HIV-positive or have unprotected sex with more than one partner, you should have a Pap test — a test that examines cells taken from the cervix — every year to check for cervical cancer, HPV and other sexually transmitted diseases. Anyone who engages in anal sex should be tested for anal cancer because HPV increases the risk of this type of cancer in both men and women.
  • Progressive multifocal leukoencephalopathy (PML). PML is an extremely serious brain infection caused by the human polyomavirus JCV. Signs and symptoms vary and may include speech problems, weakness on one side of the body, loss of vision in one eye or numbness in one arm or leg. PML usually occurs only when your immune system has been severely damaged.

Fungal infections

  • Candidiasis. Candidiasis is a common HIV-related infection. It causes inflammation and a thick white coating on the mucous membranes of your mouth, tongue (thrush), esophagus (Candida esophagitis) or vagina. Children may have especially severe symptoms in the mouth or esophagus, which can make eating painful and difficult.
  • Cryptococcal meningitis. Meningitis is an inflammation of the membranes and fluid surrounding your brain and spinal cord (meninges). Cryptococcal meningitis, the most common central nervous system infection associated with HIV, is caused by a fungus that is present in soil. Symptoms include headache, high fever, a stiff neck and sensitivity to light. Cryptococcal meningitis can be successfully treated with antifungal medications, but early treatment is essential. Meningitis is a serious disease that can cause severe complications or prove fatal in a short period of time. Once you’ve had cryptococcal meningitis, you’ll need to be on long-term medication to prevent a recurrence.

Parasitic infections

  • Pneumocystis carinii pneumonia (PCP). Although antiretroviral drugs have helped reduce the number of cases of PCP, it remains one of the most common opportunistic infections affecting people with AIDS in the United States. PCP attacks the lungs, making it difficult to breathe. Symptoms include a cough that doesn’t go away, fever and trouble breathing.
  • Toxoplasmosis. This potentially deadly infection is caused by Toxoplasma gondii, a parasite spread primarily by cats. Infected cats pass the parasites in their stools, and the parasites may then spread to other animals. Humans generally contract toxoplasmosis by touching their mouths with their hands after changing cat litter or by eating raw or undercooked meat, especially pork, lamb and venison. If you become infected with the parasites while pregnant, you may pass the infection to your baby. Once you’re infected, the parasites can spread to every organ in your body, including your heart, eyes and lungs. For many people with AIDS, toxoplasmosis leads to encephalitis, an infection of the brain. Signs and symptoms may include disorientation, seizures and difficulty walking or speaking.
  • Cryptosporidiosis. This infection is caused by an intestinal parasite that’s commonly found in animals. You contract cryptosporidiosis when you ingest contaminated food or water. The parasite grows in your intestines and bile ducts, leading to severe, chronic diarrhea in people with AIDS.


  • Kaposi’s sarcoma. Kaposi’s sarcoma is a tumor of the blood vessel walls. Although rare in people not infected with HIV, it’s common in HIV-positive people. Kaposi’s sarcoma usually appears as pink, red or purple lesions on the skin and mouth. In people with darker skin, the lesions may look dark brown or black. Kaposi’s sarcoma can also affect the internal organs, including the digestive tract and lungs. Researchers are testing new combinations of the chemotherapy drugs currently used to treat Kaposi’s sarcoma as well as new ways of delivering those medications. What’s more, as with most opportunistic infections associated with AIDS, the use of anti-retrovirals has reduced the incidence of this cancer and has even reduced the lesions in people already affected.
  • Non-Hodgkin’s lymphoma. This cancer originates in lymphocytes, a type of white blood cell. Lymphocytes are concentrated in your bone marrow, lymph nodes, spleen, digestive tract and skin. Although lymphomas can start in other organs, they usually begin in your lymph nodes. The most common early sign is painless swelling of the lymph nodes in your neck, armpit or groin.

Other complications

  • Wasting syndrome. Researchers identified wasting syndrome as a complication of AIDS in the 1980s. Although current aggressive treatment regimens have reduced the number of cases, wasting syndrome still affects many people with AIDS. It is defined as a loss of at least 10 percent of body weight and is often accompanied by diarrhea, chronic weakness and fever.
  • Neurological complications. Although AIDS doesn’t appear to infect the nerve cells, it can still cause neurological symptoms such as confusion, forgetfulness, changes in behavior, depression, anxiety and trouble walking. One of the most common neurological complications is AIDS dementia complex, which leads to behavioral changes and diminished mental functioning. It’s best treated with aggressive anti-retroviral medications.


When HIV was first identified in the early 1980s, there were few drugs to treat the virus and the opportunistic infections associated with it. Since then, a number of medications have been developed to treat both HIV/AIDS and opportunistic infections. For many people, including children, these treatments have extended and improved the quality of life. Scientists at the National Institutes of Health estimate that since 1989, anti-retroviral medications have provided HIV-positive Americans with 3 million years of extended life. But none of these drugs can cure HIV/AIDS, many have side effects that can be severe, and most are expensive. What’s more, after 20 years on AIDS drugs, some people — about 40,000 in the United States alone — develop resistance to the drugs and no longer respond to treatment. The new protease inhibitor darunavir is intended to help this group of people.

Treatment guidelines
A panel of leading AIDS specialists has developed recommendations for the use of anti-retroviral medications in people with HIV. These recommendations are based on the best information available at the time they were developed. AIDSinfo, a program of the U.S. Department of Health and Human Services, has a program in place to regularly refine and update the recommendations as knowledge about HIV infection evolves.

According to current guidelines, treatment should focus on achieving the maximum suppression of symptoms for as long as possible. This aggressive approach is known as highly active antiretroviral therapy (HAART). The aim of HAART is to reduce the amount of virus in your blood to very low, or even nondetectable, levels, although this doesn’t mean the virus is gone. This is usually accomplished with a combination of three or more drugs.

But the treatment guidelines also emphasize the importance of quality of life. Thus the goal of AIDS treatment is to find the strongest possible regimen that is also simple and has the fewest side effects. If you have HIV/AIDS, it’s important that you take an active role in every treatment decision. You and your doctor should discuss the risks and benefits of all therapies so that you can make an informed decision about what will likely be a complex and long-term treatment.

Antiretroviral drugs
Antiretroviral drugs inhibit the growth and replication of HIV at various stages of its life cycle. Six classes of these drugs are available:

  • Nucleoside analogue reverse transcriptase inhibitors (NRTIs). NRTIs were the first antiretroviral drugs to be developed. They inhibit the replication of an HIV enzyme called reverse transcriptase. They include zidovudine (Retrovir), lamivudine (Epivir) didanosine (Videx), zalcitabine (Hivid), stavudine (Zerit) and abacavir (Ziagen). A newer drug, emtricitabine (Emtriva), which must be used in combination with at least two other AIDS medications, treats both HIV and hepatitis B.

    The major side effect of zidovudine is bone marrow suppression, which causes a decrease in the number of red and white blood cells. Approximately 5 percent of people treated with abacavir experience hypersensitivity reactions such as a rash along with fever, fatigue, nausea, vomiting, diarrhea and abdominal pain. Hypersensitivity reactions can also occur without a rash. In either case, symptoms usually appear within the first six weeks of treatment and generally disappear when the drug is discontinued. If you’ve had a hypersensitivity reaction to abacavir, avoid taking the drug again. Side effects of emtricitabine include nausea, vomiting, abdominal pain, difficulty breathing and fatigue.

  • Protease inhibitors (PIs). PIs interrupt HIV replication at a later stage in its life cycle by interfering with an enzyme known as HIV protease. This causes HIV particles in your body to become structurally disorganized and noninfectious. Among these drugs are saquinavir (Invirase), ritonavir (Norvir), indinavir (Crixivan), nelfinavir (Viracept), amprenavir (Agenerase), lopinavir, atazanavir (Reyataz) and tipranavir (Aptivus). Darunavir (Prezista), a protease inhibitor approved in 2006, is intended for people who haven’t responded to treatment with other drugs. Darunavir is used in conjunction with ritonavir and other anti-HIV medications.

    The most common side effects of protease inhibitors include nausea, diarrhea and other digestive tract problems. PIs can also cause a significant number of side effects when they interact with certain other medications you may be taking. That’s because all PIs, to one degree or another, affect an enzyme system in your liver that is responsible for metabolizing a large number of drugs. Newer side effects have also appeared with the continuing and widespread use of protease inhibitors. These include elevated triglyceride levels and problems with sugar metabolism that may sometimes progress to diabetes.

    There may also be abnormalities in the way fat is metabolized and deposited in your body. Some people lose much of their total body fat; others gain excess fat on the back between their shoulders (buffalo hump) or in the stomach (protease paunch). No one knows exactly why these abnormalities occur. In fact, it’s not even certain whether these problems are a direct result of treatment with protease inhibitors or due to some other cause that has yet to be identified. Similar metabolic abnormalities have occurred in people on anti-retroviral therapy that doesn’t include PIs. Although these body changes can be distressing, the possibility they may occur should not stop you from obtaining treatment for HIV/AIDS.

  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs). These drugs bind directly to the enzyme reverse transcriptase. Four NNRTIs are approved for clinical use: nevirapine (Viramune), delavirdine (Rescriptor), efavirenz (Sustiva) and etravirine (Intelence). A major side effect of all NNRTIs is a rash. In addition, people taking efavirenz may have side effects such as abnormal dreams, sleeplessness, dizziness and difficulty concentrating.
  • Nucleotide reverse transcriptase inhibitors (NtRTIs). NtRTIs work much like nucleoside analogs: They interfere with the replication of reverse transcriptase and prevent the virus from inserting its genetic material into cells. But NtRTIs act more quickly than NRTIs do. The only approved drug in this class, tenofovir (Viread), inhibits both HIV and hepatitis B and appears to be effective in people who are resistant to NRTIs. The most common side effects of tenofovir, when used in combination with other antiretrovirals, are nausea, vomiting, diarrhea and gas. As with all reverse transcriptase inhibitors, the possibility of severe, and even fatal, liver damage exists.
  • Fusion inhibitors. One of the most alarming developments in the AIDS epidemic is the emergence of drug-resistant strains of HIV. Worldwide, a majority of people receiving treatment for HIV are resistant to at least one drug, and many don’t respond to a typical three-drug combination. But a drug called enfuvirtide (Fuzeon), the first in a new class of drugs called fusion inhibitors, appears to suppress resistant strains of HIV. Fusion inhibitors stop the virus from replicating by preventing its membrane from fusing with the membrane surrounding healthy cells. Fuzeon is used in combination with other HIV drugs for people who have advanced infection and who have developed resistance to other drugs. Doctors administer Fuzeon by injection.
  • Integrase inhibitors. The FDA approved the first drug in this new class of drugs — aimed at treating those who become resistant to other treatments — in October 2007. The drug is raltegravir (Isentress) and is intended to be used in combination with other antiretroviral drugs rather than alone. This is the first class of drugs that blocks replication of the HIV integrase enzyme, which keeps HIV DNA from inserting itself into human DNA. Common side effects include diarrhea, nausea, headache and fever.

CCR5 antagonists
CCR5 antagonists is a new class of drugs used to treat a particular type of HIV infection called CCR5-tropic HIV-1. The first drug in this class — maraviroc (Selzentry) — was approved by the FDA in August 2007 for treatment of CCR5-tropic HIV-1 in adults. Maraviroc is the first drug that targets a human protein rather than components of the HIV virus itself.

Maraviroc is used in combination with other antiretroviral drugs for the treatment of adults with CCR5-tropic HIV-1 who have elevated levels of HIV (high viral load) in their blood despite treatment with other HIV medications. Maraviroc reduces viral load by preventing HIV from entering uninfected white blood cells. It does this by blocking CCR5, a major route of entry into the cells. CCR5 is a protein found on the surface of some immune cells, and maraviroc blocks the CCR5 co-receptor from accepting HIV.

During two large clinical trials, approximately twice as many people with CCR5-tropic HIV-1 infection who received maraviroc had undetectable viral loads after 24 weeks as did those who received more standard therapy in the control groups.

Side effects of maraviroc may include liver and cardiovascular problems, as well as cough, fever, upper respiratory tract infections, rash and abdominal pain.

Treatment response
Your response to any treatment is measured by viral load. Viral load should be tested at the start of treatment and then every three to four months while you’re on therapy. In some cases you may be tested even more often.

New treatments
Many new drugs for HIV- or AIDS-related infections are in development or being tested in clinical trials. Among them is a drug that attacks the virus in the last stage of its life cycle. Although these medications are not yet licensed, some may be available by compassionate exception to people who need them.

Experts predict that an AIDS vaccine probably won’t be found soon. More promising is the search for a microbicide to protect women from HIV infection during sex. Although microbicides may never be as effective as condoms, which offer nearly 100 percent protection when used properly, a microbicide could still save millions of lives.

For more information on new therapies, call AIDSinfo at 800-TRIALS-A, or 800-874-2572.



There’s no vaccine to prevent HIV infection and no cure for AIDS. But it’s possible to protect yourself and others from infection. That means educating yourself about HIV and avoiding any behavior that allows HIV-infected fluids — blood, semen, vaginal secretions and breast milk — into your body.

If you’re HIV-negative
The following measures can help keep you from being infected with HIV:

  • Educate yourself and others. Make sure you understand what HIV is and how the virus is transmitted. Just as important, teach your children about HIV.
  • Know the HIV status of any sexual partner. Don’t engage in unprotected sex unless you’re absolutely certain your partner isn’t infected with HIV.
  • Use a new latex or polyurethane condom every time you have sex. If you don’t know the HIV status of your partner, use a new latex condom every time you have anal or vaginal sex. If you’re allergic to latex, use a plastic (polyurethane) condom. Avoid lambskin condoms — they do not protect you from HIV. If you don’t have a male condom, use a female condom. Use only water-based lubricants, not petroleum jelly, cold cream or oils. Oil-based lubricants can weaken condoms and cause them to break. During oral sex use a condom,dental dam — a piece of medical-grade latex —or plastic wrap. Remember that although condoms can reduce your risk of contracting HIV, they don’t eliminate the risk entirely. Condoms can break or develop small tears, and they may not always be used properly.
  • Consider male circumcision. A large study in 2006 by the National Institutes of Health showed that medically performed circumcision significantly reduced a man’s risk of acquiring HIV through heterosexual intercourse. The study, conducted in Kenya, showed a 53 percent reduction of HIV infection in circumcised HIV-negative men compared with uncircumcised men in the study. The outcome was heralded by the NIH as good news not only because it reduced the number of HIV-infected men, but also because it could lead to fewer infections among women in areas of the world where HIV is spread primarily through heterosexual intercourse.
  • Use a clean needle. If you use a needle to inject drugs, make sure it’s sterile, and don’t share it. Take advantage of needle exchange programs in your community and consider seeking help for your drug use.
  • Be cautious about blood products in certain countries. Although the blood supply in the United States is now well screened, this isn’t always the case in other countries. If an emergency requires that you receive blood or blood products in another country, get tested for HIV as soon as you return home.
  • Get regular screening tests. If you are a woman, have a yearly Pap test. Men and women who engage in anal sex should also have regular tests for anal cancer.
  • Don’t become complacent. Because potent antiretroviral medications have reduced the number of AIDS deaths in the United States, you may think that HIV infection is no longer a problem. But HIV/AIDS is still a terminal illness for which there is no vaccine and no cure. Right now, the only way to stay healthy is to protect yourself and others from infection.

If you’re HIV-positive
If you’ve received a diagnosis of HIV/AIDS, the following guidelines can help protect others:

  • Follow safe sex practices. The only foolproof way to protect others from infection is to avoid practices that expose them to blood, semen or vaginal secretions. Barring that, carefully follow guidelines for safe sex, including using a new latex condom every time you have vaginal or anal sex and using a dental dam, condom or piece of plastic wrap during oral sex. If you use sexual devices, don’t share them. It’s also important to avoid having unprotected sex with other HIV-positive people because of the risk of acquiring or passing on a drug-resistant strain of the virus.
  • Tell your sexual partner(s) you have HIV. It’s important to tell anyone with whom you’ve had sex that you’re HIV-positive. Your partners need to be tested and to receive medical care if they have the virus. They also need to know their HIV status so that they don’t infect others.
  • If your partner is pregnant, tell her you have HIV. Even if you’re not the father, be sure to tell any pregnant woman with whom you’ve had sex that you’re HIV-positive. She needs to receive treatment to protect her own health and that of her baby.
  • Tell others who need to know. Although only you can decide whether to tell friends and family about your illness, you do need to inform your health care providers of your HIV status. This is not just to protect them, but also to ensure that you get the best possible medical care.
  • Don’t share needles or syringes. If you use intravenous drugs, never share your needles and syringes.
  • Don’t donate blood or organs. The virus will spread to other people.
  • Don’t share razor blades or toothbrushes. These items may carry traces of HIV-infected blood.
  • If you’re pregnant, get medical care right away. If you’re HIV-positive, you may pass the infection to your baby. But if you receive treatment during pregnancy, you can cut your baby’s risk by as much as two-thirds.



Although it’s important to receive medical treatment for HIV/AIDS, it’s also essential to take an active role in your own care. The following suggestions may help you stay healthy longer:

  • Make sure your doctor knows how to treat HIV. Find someone who understands all the ramifications of the disease. You’ll also want a doctor who is willing to work with you and who makes you feel comfortable and respected.
  • Follow your doctor’s instructions. Keep all of your appointments, and take your medications exactly as directed. Many treatment regimens are much simpler now than in the past — some requiring as few as one pill a day. Even so, sticking with treatment can be difficult. If you get sick from your medication, call your doctor. Don’t stop taking your medication or change the dosage on your own.
  • Get immunizations. These may prevent infections such as pneumonia and the flu.
  • Don’t smoke or use illegal drugs. These weaken your body even more.
  • Eat the healthiest diet you can. Emphasize fresh fruits and vegetables, whole grains and lean protein. Healthy foods help keep you strong, give you more energy and support your immune system. Unfortunately, you may not always feel like eating when you have HIV. But good nutrition is tremendously important. A registered dietitian can be especially helpful if you have diarrhea, weight loss or trouble eating. Also, because your nutritional needs are extremely high and you may not digest food well, talk to your doctor about vitamin and mineral supplements.
  • Avoid foods that may put you at risk of infection. These include unpasteurized dairy products, raw eggs and raw seafood such as oysters, sushi or sashimi. Cook meat until it’s well-done or until there’s no trace of pink color.
  • Drink pure water. The Department of Health and Human Services recommends that you boil tap water or use bottled or filtered water for drinking. If you buy a water filter, look for one that uses reverse osmosis as part of the purification process.
  • Get regular exercise. Exercise helps increase your strength and energy levels and can help battle the depression that’s often a part of dealing with HIV/AIDS.
  • Get enough sleep. Rest when you need to.
  • Take care with companion animals. Some animals may carry parasites that can cause infections in people who are HIV-positive. But that doesn’t mean you should give up your companion animal. You can protect yourself by having someone else clean your cat’s litter box or pick up after your dog. If you must do these chores yourself, wear latex gloves and wash your hands immediately afterward. Don’t feed your pets raw meat, and make sure they have all their shots. Always wash your hands thoroughly with soap and water after petting or playing with your animals.
  • Find ways to relax. This might mean anything from yoga or meditation to walking, reading, playing chess or computer games, or listening to music.
  • Keep your hands clean. Wash your hands thoroughly with soap and water after using the restroom, before eating or preparing food, and after spending time in public places. You might find it helpful to carry an alcohol-based hand sanitizer with you for times when it’s not convenient to use soap and water.

Coping skills

Receiving a diagnosis of any life-threatening illness is devastating. But the emotional, social and financial consequences of HIV/AIDS can make coping with this illness especially difficult — not only for you but also for those closest to you.

Fortunately, a wide range of services and resources are available to people with HIV. Most HIV/AIDS clinics have social workers, counselors or nurses who can help you with problems directly or put you in touch with people who can. All have experience with HIV and are there to help you with the large part of your life that lies beyond medicine. They can arrange for transportation to and from doctor appointments, help with housing and child care, deal with employment and legal issues, and see you through financial emergencies.

Treatment for HIV presents its own problems. The regimens are sometimes complicated and side effects can be severe. Furthermore, the physical effects of treatment can create difficulties in other areas of your life. You may have a hard time explaining to your employer why you’re sick so often or have so many doctor visits, for example. You also may not be able to participate in life as fully as you’d like.

Some of the following suggestions may help you deal with the emotional toll of living with HIV/AIDS:

  • Learn all you can about HIV/AIDS. Find out how the disease progresses, your prognosis and your treatment options, including both experimental and standard treatments and their side effects. The more you know, the more active you can be in your own care.
  • Be proactive. Although you may often feel tired and discouraged, don’t let others — including your family or your doctor — make important decisions for you. It’s vital that you take an active role in your treatment.
  • Maintain a strong support system. Strong relationships are crucial in dealing with life-threatening illnesses. Although friends and family can be your best allies, in some cases they may have trouble dealing with your illness. If so, an HIV counselor, other people who are HIV-positive, or a formal support group may be especially helpful.
  • Take time to make important decisions. One intense struggle you’ll likely face is how much to reveal about your illness. When your disease is first diagnosed, you may not want anyone to know. But HIV/AIDS is a terrible burden to carry alone. Like many people, you may eventually decide that it’s important for your emotional well-being to confide in someone you trust. The choice is up to you. You need to tell your current and former sexual partners and your health care providers. Beyond that, there is no legal obligation for you to reveal your HIV status, even to your employer. In fact, the law guarantees your right to privacy.
  • Come to terms with your illness. Coming to terms with your illness may be the hardest thing you’ve ever done. For some people, having a strong faith or a sense of something greater than themselves makes this process easier. Others seek counseling from someone who understands HIV/AIDS. Still others make a conscious decision to experience their lives as fully and intensely as they can or to help other people who have the disease. A vast support network is available for people with HIV infection.


Complementary and alternative medicine

Be sure to discuss any alternative treatments you may be using with your doctor. Some may interfere or interact with other medications you’re taking. The herb St. John’s wort, for instance, can interfere with the effectiveness of antiretroviral medications.

On the other hand, complementary treatments such as acupuncture can help relieve pain, fatigue and side effects of medication such as nausea and vomiting; strengthen the immune system; and reduce stress. If you’re interested in finding out more about alternative and complementary treatments, many resources are available both on and off the Internet.

Posted in POZ World View | 3 Comments »

HIV – Wikipedia, the free encyclopedia

Posted by pozlife on May 26, 2008


Human immunodeficiency virus (HIV) is a retrovirus that can lead to acquired immunodeficiency syndrome (AIDS), a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections. Previous names for the virus include human T-lymphotropic virus-III (HTLV-III), lymphadenopathy-associated virus (LAV), and AIDS-associated retrovirus (ARV).[1][2]

Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. The four major routes of transmission are unprotected sexual intercourse, contaminated needles, breast milk, and transmission from an infected mother to her baby at birth. Screening of blood products for HIV has largely eliminated transmission through blood transfusions or infected blood products in the developed world.

HIV infection in humans is now pandemic. As of January 2006, the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on December 1, 1981, making it one of the most destructive pandemics in recorded history. It is estimated that about 0.6% of the world’s population is infected with HIV.[3][update needed] In 2005 alone, AIDS claimed an estimated 2.4–3.3 million lives, of which more than 570,000 were children. A third of these deaths are occurring in sub-Saharan Africa, retarding economic growth and increasing poverty.[4][dead link] According to current estimates, HIV is set to infect 90 million people in Africa, resulting in a minimum estimate of 18 million orphans.[5] Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but routine access to antiretroviral medication is not available in all countries.[6]

HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages and dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosis in infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.

Eventually most HIV-infected individuals develop AIDS (Acquired Immunodeficiency Syndrome). These individuals mostly die from opportunistic infections or malignancies associated with the progressive failure of the immune system.[7] About 9 out of every 10 persons with HIV will progress to AIDS after 10-15 years.[8] Treatment with anti-retrovirals, where available, increases the life expectancy of people infected with HIV. After the diagnosis of AIDS is made, the current average survival time with antiretroviral therapy (as of 2005) is estimated to be more than 5 years.[9] Without antiretroviral therapy, death normally occurs within a year.[10] It is hoped that current and future treatments may allow HIV-infected individuals to achieve a life expectancy approaching that of the general public.


HIV is a member of the genus Lentivirus,[11] part of the family of Retroviridae.[12] Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.[13] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase, along with host cellular co-factors[14], so that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Two species of HIV infect humans: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed LAV. It is more virulent, relatively easily transmitted, and is the cause of the majority of HIV infections globally. HIV-2 is less transmittable than HIV-1 and is largely confined to West Africa.[15]

Comparison of HIV species

Purported origin

Common Chimpanzee

West Africa
Sooty Mangabey


Controversy surrounding the discovery of the Human Immunodeficiency Virus (HIV) was intense after American researcher Robert Gallo and French scientist Luc Montagnier both claimed to have discovered it. The dispute was settled on a political level with both teams receiving equal credit.


Estimated per act risk for acquisition
of HIV-1 by exposure route[16]

Exposure Route
Estimated infections
per 10,000 exposures
to an infected source

Blood Transfusion


Needle-sharing injection drug use

Receptive anal intercourse*

Percutaneous needle stick

Receptive penile-vaginal intercourse*

Insertive anal intercourse*

Insertive penile-vaginal intercourse*

Receptive fellatio*

Insertive fellatio*

* assuming no condom use

Since the beginning of the pandemic, three main transmission routes for HIV have been identified:

  • Sexual route. The majority of HIV infections are acquired through unprotected sexual relations. Sexual transmission can occur when infected sexual secretions of one partner come into contact with the genital, oral, or rectal mucous membranes of another.
  • Blood or blood product route. This transmission route can account for infections in intravenous drug users, hemophiliacs and recipients of blood transfusions (though most transfusions are checked for HIV in the developed world) and blood products. It is also of concern for persons receiving medical care in regions where there is prevalent substandard hygiene in the use of injection equipment, such as the reuse of needles in Third World countries. HIV can also be spread through the sharing of needles. Health care workers such as nurses, laboratory workers, and doctors, have also been infected, although this occurs more rarely. People who give and receive tattoos, piercings, and scarification procedures can also be at risk of infection.
  • Mother-to-child transmission (MTCT). The transmission of the virus from the mother to the child can occur in utero during pregnancy and intrapartum at childbirth. In the absence of treatment, the transmission rate between the mother and child is around 25%.[18] However, where combination antiretroviral drug treatment and Cesarian section are available, this risk can be reduced to as low as 1%.[18] Breast feeding also presents a risk of infection for the baby.

HIV-2 is transmitted much less frequently by the MTCT and sexual route than HIV-1.

HIV has been found at low concentrations in the saliva, tears and urine of infected individuals, but there are no recorded cases of infection by these secretions and the potential risk of transmission is negligible.[24] The use of physical barriers such as the latex condom is widely advocated to reduce the sexual transmission of HIV. Spermicide, when used alone or with vaginal contraceptives like a diaphragm, actually increases the male to female transmission rate due to inflammation of the vagina; it should not be considered a barrier to infection.[25]

A meta-analysis of twenty-seven observational studies conducted prior to 1999 in sub-Saharan Africa indicated that male circumcision reduces the risk of HIV infection.[26] However, a subsequent review indicated that the correlation between circumcision and HIV in these observational studies may have been due to confounding factors.[27] Later trials, in which uncircumcised men were randomly assigned to be medically circumcised in sterile conditions and given counseling and other men were not circumcised, have been conducted in South Africa,[28] Kenya[29] and Uganda[30] showing reductions in HIV transmission for heterosexual sex of 60%, 53%, and 51% respectively. As a result, a panel of experts convened by WHO and the UNAIDS Secretariat has “recommended that male circumcision now be recognized as an additional important intervention to reduce the risk of heterosexually acquired HIV infection in men.”[31] Research is clarifying whether there is a historical relationship between rates of male circumcision and rates of HIV in differing social and cultural contexts. Some South African medical experts have expressed concern that the repeated use of unsterilized blades in the ritual (not medical) circumcision of adolescent boys may be spreading HIV.[32]

Structure and genome

Main article: HIV structure and genome

Diagram of HIV

Diagram of HIV

HIV is different in structure from other retroviruses. It is about 120 nm in diameter (120 billionths of a meter; around 60 times smaller than a red blood cell, yet large for being a virus [33]) and roughly spherical.[34] It is composed of two copies of positive single-stranded RNA that codes for the virus’s nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24.[35][dead link] The single-stranded RNA is tightly bound to nucleocapsid proteins, p7 and enzymes needed for the development of the virion such as reverse transcriptase, proteases, ribonuclease and integrase. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle.[35] This is, in turn, surrounded by the viral envelope which is composed of two layers of fatty molecules called phospholipids taken from the membrane of a human cell when a newly formed virus particle buds from the cell. Embedded in the viral envelope are proteins from the host cell and about 70 copies of a complex HIV protein that protrudes through the surface of the virus particle.[35] This protein, known as Env, consists of a cap made of three molecules called glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope.[36] This glycoprotein complex enables the virus to attach to and fuse with target cells to initiate the infectious cycle.[36] Both these surface proteins, especially gp120, have been considered as targets of future treatments or vaccines against HIV.[37]

Of the nine genes that are encoded within the RNA genome, three of these genes, gag, pol, and env, contain information needed to make the structural proteins for new virus particles.[35] For example, env codes for a protein called gp160 that is broken down by a viral enzyme to form gp120 and gp41. The six remaining genes, tat, rev, nef, vif, vpr, and vpu (or vpx in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease.[35] The protein encoded by nef, for instance, appears necessary for the virus to replicate efficiently, and the vpu-encoded protein influences the release of new virus particles from infected cells.[35] The ends of each strand of HIV RNA contain an RNA sequence called the long terminal repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell.[35]


Main article: HIV tropism

The term viral tropism refers to which cell types HIV infects. HIV can infect a variety of immune cells such as CD4+ T cells, macrophages, and microglial cells. HIV-1 entry to macrophages and CD4+ T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells and also with chemokine coreceptors.[36]

Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the β-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T cells.[38] This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV infection. They appear to be the first cells infected by HIV and perhaps the source of HIV production when CD4+ cells become depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.

T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4+ T cells as well as in macrophages and use the α-chemokine receptor, CXCR4, for entry.[38][39][40] Dual-tropic HIV-1 strains are thought to be transitional strains of the HIV-1 virus and thus are able to use both CCR5 and CXCR4 as co-receptors for viral entry.

The α-chemokine, SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down-regulating the expression of CXCR4 on the surface of these cells. HIV that use only the CCR5 receptor are termed R5, those that only use CXCR4 are termed X4, and those that use both, X4R5. However, the use of coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection[38] and HIV can also infect a subtype of myeloid dendritic cells,[41] which probably constitute a reservoir that maintains infection when CD4+ T cell numbers have declined to extremely low levels.

Some people are resistant to certain strains of HIV.[42] One example of how this occurs is people with the CCR5-Δ32 mutation; these people are resistant to infection with R5 virus as the mutation stops HIV from binding to this coreceptor, reducing its ability to infect target cells.

Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid which is passed from partner to partner. The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process leads to a predominant transmission of the R5 virus through this pathway.[43][44][45] How this selective process works is still under investigation, but one model is that spermatozoa may selectively carry R5 HIV as they possess both CCR3 and CCR5 but not CXCR4 on their surface[46] and that genital epithelial cells preferentially sequester X4 virus.[47] In patients infected with subtype B HIV-1, there is often a co-receptor switch in late-stage disease and T-tropic variants appear that can infect a variety of T cells through CXCR4.[48] These variants then replicate more aggressively with heightened virulence that causes rapid T cell depletion, immune system collapse, and opportunistic infections that mark the advent of AIDS.[49] Thus, during the course of infection, viral adaptation to the use of CXCR4 instead of CCR5 may be a key step in the progression to AIDS. A number of studies with subtype B-infected individuals have determined that between 40 and 50% of AIDS patients can harbour viruses of the SI, and presumably the X4, phenotype.[50][51]

Replication cycle

The HIV replication cycle

The HIV replication cycle

Entry to the cell

HIV enters macrophages and CD4+ T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell.[52][53]

Entry to the cell begins through interaction of the trimeric envelope complex (gp160 spike) and both CD4 and a chemokine receptor (generally either CCR5 or CXCR4, but others are known to interact) on the cell surface.[52][53] gp120 binds to integrin α4β7 activating LFA-1 the central integrin involved in the establishment of virological synapses, which facilitate efficient cell-to-cell spreading of HIV-1.[54] The gp160 spike contains binding domains for both CD4 and chemokine receptors.[52][53] The first step in fusion involves the high-affinity attachment of the CD4 binding domains of gp120 to CD4. Once gp120 is bound with the CD4 protein, the envelope complex undergoes a structural change, exposing the chemokine binding domains of gp120 and allowing them to interact with the target chemokine receptor.[52][53] This allows for a more stable two-pronged attachment, which allows the N-terminal fusion peptide gp41 to penetrate the cell membrane.[52][53] Repeat sequences in gp41, HR1 and HR2 then interact, causing the collapse of the extracellular portion of gp41 into a hairpin. This loop structure brings the virus and cell membranes close together, allowing fusion of the membranes and subsequent entry of the viral capsid.[52][53]

Once HIV has bound to the target cell, the HIV RNA and various enzymes, including reverse transcriptase, integrase, ribonuclease and protease, are injected into the cell.[52] During the microtubule based transport to the nucleus, the viral single strand RNA genome is transcribed into double strand DNA, which is then integrated into a host chromosome.

HIV can infect dendritic cells (DCs) by this CD4-CCR5 route, but another route using mannose-specific C-type lectin receptors such as DC-SIGN can also be used.[55] DCs are one of the first cells encountered by the virus during sexual transmission. They are currently thought to play an important role by transmitting HIV to T cells once the virus has been captured in the mucosa by DCs.[55]

Replication and transcription

Once the viral capsid enters the cell, an enzyme called reverse transcriptase liberates the single-stranded (+)RNA from the attached viral proteins and copies it into a complementary DNA.[56] This process of reverse transcription is extremely error-prone and it is during this step that mutations may occur. Such mutations may cause drug resistance. The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA intermediate (vDNA). This vDNA is then transported into the cell nucleus. The integration of the viral DNA into the host cell’s genome is carried out by another viral enzyme called integrase.[56]

Reverse transcription of the HIV genome into double strand DNA

Reverse transcription of the HIV genome into double strand DNA

This integrated viral DNA may then lie dormant, in the latent stage of HIV infection.[56] To actively produce the virus, certain cellular transcription factors need to be present, the most important of which is NF-κB (NF kappa B), which is upregulated when T cells become activated.[57] This means that those cells most likely to be killed by HIV are those currently fighting infection.

In this replication process, the integrated provirus is copied to mRNA which is then spliced into smaller pieces. These small pieces produce the regulatory proteins Tat (which encourages new virus production) and Rev. As Rev accumulates it gradually starts to inhibit mRNA splicing.[58] At this stage, the structural proteins Gag and Env are produced from the full-length mRNA. The full-length RNA is actually the virus genome; it binds to the Gag protein and is packaged into new virus particles.

HIV-1 and HIV-2 appear to package their RNA differently; HIV-1 will bind to any appropriate RNA whereas HIV-2 will preferentially bind to the mRNA which was used to create the Gag protein itself. This may mean that HIV-1 is better able to mutate (HIV-1 infection progresses to AIDS faster than HIV-2 infection and is responsible for the majority of global infections).

Assembly and release

The final step of the viral cycle, assembly of new HIV-1 virons, begins at the plasma membrane of the host cell. The Env polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi complex where it is cleaved by protease and processed into the two HIV envelope glycoproteins gp41 and gp120. These are transported to the plasma membrane of the host cell where gp41 anchors the gp120 to the membrane of the infected cell. The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell. Maturation either occurs in the forming bud or in the immature virion after it buds from the host cell. During maturation, HIV proteases cleave the polyproteins into individual functional HIV proteins and enzymes. The various structural components then assemble to produce a mature HIV virion.[59][dead link] This cleavage step can be inhibited by protease inhibitors. The mature virus is then able to infect another cell.

Genetic variability

Further information: Subtypes of HIV

The phylogenetic tree of the SIV and HIV.

The phylogenetic tree of the SIV and HIV.

HIV differs from many viruses in that it has very high genetic variability. This diversity is a result of its fast replication cycle, with the generation of 109 to 1010 virions every day, coupled with a high mutation rate of approximately 3 x 10-5 per nucleotide base per cycle of replication and recombinogenic properties of reverse transcriptase.[60] This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day.[60] This variability is compounded when a single cell is simultaneously infected by two or more different strains of HIV. When simultaneous infection occurs, the genome of progeny virions may be composed of RNA strands from two different strains. This hybrid virion then infects a new cell where it undergoes replication. As this happens, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes.[60] This recombination is most obvious when it occurs between subtypes.[60]

The closely related simian immunodeficiency virus (SIV) exhibits a somewhat different behavior: in its natural hosts, African green monkeys and sooty mangabeys, the retrovirus is present in high levels in the blood, but evokes only a mild immune response,[61] does not cause the development of simian AIDS,[62] and does not undergo the extensive mutation and recombination typical of HIV.[63] By contrast, infection of heterologous hosts (rhesus or cynomologus macaques) with SIV results in the generation of genetic diversity that is on the same order as HIV in infected humans; these heterologous hosts also develop simian AIDS.[64] The relationship, if any, between genetic diversification, immune response, and disease progression is unknown.

Three groups of HIV-1 have been identified on the basis of differences in env: M, N, and O.[65] Group M is the most prevalent and is subdivided into eight subtypes (or clades), based on the whole genome, which are geographically distinct.[66] The most prevalent are subtypes B (found mainly in North America and Europe), A and D (found mainly in Africa), and C (found mainly in Africa and Asia); these subtypes form branches in the phylogenetic tree representing the lineage of the M group of HIV-1. Coinfection with distinct subtypes gives rise to circulating recombinant forms (CRFs). In 2000, the last year in which an analysis of global subtype prevalence was made, 47.2% of infections worldwide were of subtype C, 26.7% were of subtype A/CRF02_AG, 12.3% were of subtype B, 5.3% were of subtype D, 3.2% were of CRF_AE, and the remaining 5.3% were composed of other subtypes and CRFs.[67] Most HIV-1 research is focused on subtype B; few laboratories focus on the other subtypes.[68]

The genetic sequence of HIV-2 is only partially homologous to HIV-1 and more closely resembles that of SIV than HIV-1.

The clinical course of infection

A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection; any particular individual's disease course may vary considerably.                      CD4+ T cell count (cells per µL)                      HIV RNA copies per mL of plasma

A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection; any particular individual’s disease course may vary considerably. CD4+ T cell count (cells per µL) HIV RNA copies per mL of plasma

Infection with HIV-1 is associated with a progressive decrease of the CD4+ T cell count and an increase in viral load. The stage of infection can be determined by measuring the patient’s CD4+ T cell count, and the level of HIV in the blood.

HIV infection has basically four stages: incubation period, acute infection, latency stage and AIDS. The initial incubation period upon infection is asymptomatic and usually lasts between two and four weeks. The second stage, acute infection, which lasts an average of 28 days and can include symptoms such as fever, lymphadenopathy (swollen lymph nodes), pharyngitis (sore throat), rash, myalgia (muscle pain), malaise, and mouth and esophageal sores. The latency stage, which occurs third, shows few or no symptoms and can last anywhere from two weeks to twenty years and beyond. AIDS, the fourth and final stage of HIV infection shows as symptoms of various opportunistic infections.

Acute HIV infection

Main article: Acute HIV infection

The initial infection with HIV generally occurs after transfer of body fluids from an infected person to an uninfected one. The first stage of infection, the primary, or acute infection, is a period of rapid viral replication that immediately follows the individual’s exposure to HIV leading to an abundance of virus in the peripheral blood with levels of HIV commonly approaching several million viruses per mL.[69] This response is accompanied by a marked drop in the numbers of circulating CD4+ T cells. This acute viremia is associated in virtually all patients with the activation of CD8+ T cells, which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8+ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4+ T cell counts rebound to around 800 cells per mL (the normal blood value is 1200 cells per mL ). A good CD8+ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus.[70] During this period (usually 2-4 weeks post-exposure) most individuals (80 to 90%) develop an influenza or mononucleosis-like illness called acute HIV infection, the most common symptoms of which may include fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, mouth and esophagal sores, and may also include, but less commonly, headache, nausea and vomiting, enlarged liver/spleen, weight loss, thrush, and neurological symptoms. Infected individuals may experience all, some, or none of these symptoms. The duration of symptoms varies, averaging 28 days and usually lasting at least a week.[71] Because of the nonspecific nature of these symptoms, they are often not recognized as signs of HIV infection. Even if patients go to their doctors or a hospital, they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. Consequently, these primary symptoms are not used to diagnose HIV infection as they do not develop in all cases and because many are caused by other more common diseases. However, recognizing the syndrome can be important because the patient is much more infectious during this period. [72]

Latency stage

A strong immune defense reduces the number of viral particles in the blood stream, marking the start of the infection’s clinical latency stage. Clinical latency can vary between two weeks and 20 years. During this early phase of infection, HIV is active within lymphoid organs, where large amounts of virus become trapped in the follicular dendritic cells (FDC) network.[73] The surrounding tissues that are rich in CD4+ T cells may also become infected, and viral particles accumulate both in infected cells and as free virus. Individuals who are in this phase are still infectious. During this time, CD4+ CD45RO+ T cells carry most of the proviral load.[74]


Main article: AIDS

For more details on this topic, see AIDS Diagnosis, AIDS Symptoms and WHO Disease Staging System for HIV Infection and Disease

When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and infections with a variety of opportunistic microbes appear. The first symptoms often include moderate and unexplained weight loss, recurring respiratory tract infections (such as sinusitis, bronchitis, otitis media, pharyngitis), prostatitis, skin rashes, and oral ulcerations. Common opportunistic infections and tumors, most of which are normally controlled by robust CD4+ T cell-mediated immunity then start to affect the patient. Typically, resistance is lost early on to oral Candida species and to Mycobacterium tuberculosis, which leads to an increased susceptibility to oral candidiasis (thrush) and tuberculosis. Later, reactivation of latent herpes viruses may cause worsening recurrences of herpes simplex eruptions, shingles, Epstein-Barr virus-induced B-cell lymphomas, or Kaposi’s sarcoma, a tumor of endothelial cells that occurs when HIV proteins such as Tat interact with Human Herpesvirus-8. Pneumonia caused by the fungus Pneumocystis jirovecii is common and often fatal. In the final stages of AIDS, infection with cytomegalovirus (another herpes virus) or Mycobacterium avium complex is more prominent. Not all patients with AIDS get all these infections or tumors, and there are other tumors and infections that are less prominent but still significant.

HIV test

Main article: HIV test

Many HIV-positive people are unaware that they are infected with the virus.[75] For example, less than 1% of the sexually active urban population in Africa have been tested and this proportion is even lower in rural populations.[75] Furthermore, only 0.5% of pregnant women attending urban health facilities are counselled, tested or receive their test results.[75] Again, this proportion is even lower in rural health facilities.[75] Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.[76]

HIV-1 testing consists of initial screening with an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a nonreactive result from the initial ELISA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate.[77] If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., Western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are considered HIV-positive and indicative of HIV infection. Specimens that are repeatedly ELISA-reactive occasionally provide an indeterminate Western blot result, which may be either an incomplete antibody response to HIV in an infected person, or nonspecific reactions in an uninfected person.[78] Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. Generally, a second specimen should be collected more than a month later and retested for persons with indeterminate Western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations.[77] In addition, a few tested specimens might provide inconclusive results because of a low quantity specimen. In these situations, a second specimen is collected and tested for HIV infection.


See also Antiretroviral drug.

Abacavir - a nucleoside analog reverse transcriptase inhibitors (NARTIs or NRTIs)

Abacavir – a nucleoside analog reverse transcriptase inhibitors (NARTIs or NRTIs)

There is currently no vaccine or cure for HIV or AIDS. The only known method of prevention is avoiding exposure to the virus. However, an antiretroviral treatment, known as post-exposure prophylaxis, is believed to reduce the risk of infection if begun directly after exposure.[79] Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART.[80] This has been highly beneficial to many HIV-infected individuals since its introduction in 1996, when the protease inhibitor-based HAART initially became available.[81] Current HAART options are combinations (or “cocktails”) consisting of at least three drugs belonging to at least two types, or “classes,” of antiretroviral agents. Typically, these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because AIDS progression in children is more rapid and less predictable than in adults, particularly in young infants, more aggressive treatment is recommended for children than adults.[82] In developed countries where HAART is available, doctors assess their patients thoroughly: measuring the viral load, how fast CD4 declines, and patient readiness. They then decide when to recommend starting treatment.[83]

HAART allows the stabilisation of the patient’s symptoms and viremia, but it neither cures the patient, nor alleviates the symptoms; high levels of HIV-1, often HAART resistant, return once treatment is stopped.[84][85] Moreover, it would take more than a lifetime for HIV infection to be cleared using HAART.[86] Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to a large reduction in HIV-associated morbidity and mortality in the developed world.[81][87][88] The average life expectancy of an HIV infected individual is 32 years from the time of infection if treatment is started when the CD4 count is 350/µL.[89] The study predicting this was, however, limited as it did not take into account possible future treatments and the projection has not been confirmed within a clinical cohort setting. In the absence of HAART, progression from HIV infection to AIDS has been observed to occur at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.[10] However, HAART sometimes achieves far less than optimal results, in some circumstances being effective in less than fifty percent of patients. This is due to a variety of reasons such as medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. However, non-adherence and non-persistence with antiretroviral therapy is the major reason most individuals fail to benefit from HAART.[90] The reasons for non-adherence and non-persistence with HAART are varied and overlapping. Major psychosocial issues, such as poor access to medical care, inadequate social supports, psychiatric disease and drug abuse contribute to non-adherence. The complexity of these HAART regimens, whether due to pill number, dosing frequency, meal restrictions or other issues along with side effects that create intentional non-adherence also contribute to this problem.[91][92][93] The side effects include lipodystrophy, dyslipidemia, insulin resistance, an increase in cardiovascular risks and birth defects.[94][95]

The timing for starting HIV treatment is still debated. There is no question that treatment should be started before the patient’s CD4 count falls below 200, and most national guidelines say to start treatment once the CD4 count falls below 350; but there is some evidence from cohort studies that treatment should be started before the CD4 count falls below 350.[96][87] In those countries where CD4 counts are not available, patients with WHO stage III or IV disease[97] should be offered treatment.

Anti-retroviral drugs are expensive, and the majority of the world’s infected individuals do not have access to medications and treatments for HIV and AIDS.[98] Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. Unfortunately, only a vaccine is thought to be able to halt the pandemic. This is because a vaccine would cost less, thus being affordable for developing countries, and would not require daily treatment.[98] However, after over 20 years of research, HIV-1 remains a difficult target for a vaccine.[98] A region on HIV’s surface is a potential target for a vaccine.[99]

Promising new treatments include Cre recombinase [100] and the enzyme Tre recombinase[101], both of which are able to remove HIV from an infected cell. These enzymes promise a treatment in which a patient’s stem cells are extracted, cured, and reinjected to promulgate the enzyme into the body. The carried enzyme then finds and removes the virus.


Main article: AIDS pandemic

Estimated prevalence of HIV among young adults (15-49) per country at the end of 2005.

Estimated prevalence of HIV among young adults (15-49) per country at the end of 2005.

UNAIDS and the WHO estimate that AIDS has killed more than 25 million people since it was first recognized in 1981, making it one of the most destructive pandemics in recorded history. Despite recent improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.8 million (between 2.4 and 3.3 million) lives in 2005 of which more than half a million (570,000) were children.[3]

Globally, between 33.4 and 46 million people currently live with HIV.[3] In 2005, between 3.4 and 6.2 million people were newly infected and between 2.4 and 3.3 million people with AIDS died, an increase from 2004 and the highest number since 1981.

Sub-Saharan Africa remains by far the worst-affected region, with an estimated 21.6 to 27.4 million people currently living with HIV. Two million [1.5–3.0 million] of them are children younger than 15 years of age. More than 64% of all people living with HIV are in sub-Saharan Africa, as are more than three quarters of all women living with HIV. In 2005, there were 12.0 million [10.6–13.6 million] AIDS orphans living in sub-Saharan Africa 2005.[3] South & South East Asia are second-worst affected with 15% of the total. AIDS accounts for the deaths of 500,000 children in this region. South Africa has the largest number of HIV patients in the world followed by Nigeria.[102] India has an estimated 2.5  million infections (0.23% of population), making India the country with the third largest population of HIV patients. In the 35 African nations with the highest prevalence, average life expectancy is 48.3 years—6.5 years less than it would be without the disease.[103]

The latest evaluation report of the World Bank’s Operations Evaluation Department assesses the development effectiveness of the World Bank’s country-level HIV/AIDS assistance defined as policy dialogue, analytic work, and lending with the explicit objective of reducing the scope or impact of the AIDS epidemic.[104] This is the first comprehensive evaluation of the World Bank’s HIV/AIDS support to countries, from the beginning of the epidemic through mid-2004. Because the Bank aims to assist in implementation of national government programmes, their experience provides important insights on how national AIDS programmes can be made more effective.

The development of HAART as effective therapy for HIV infection and AIDS has substantially reduced the death rate from this disease in those areas where these drugs are widely available. This has created the misperception that the disease has vanished. In fact, as the life expectancy of persons with AIDS has increased in countries where HAART is widely used, the number of persons living with AIDS has increased substantially. In the United States, the number of persons with AIDS increased from about 35,000 in 1988 to over 220,000 in 1996.[105][dead link]

In Africa, the number of MTCT and the prevalence of AIDS is beginning to reverse decades of steady progress in child survival. Countries such as Uganda are attempting to curb the MTCT epidemic by offering VCT (voluntary counselling and testing), PMTCT (prevention of mother-to-child transmission) and ANC (ante-natal care) services, which include the distribution of antiretroviral therapy.



Main article: AIDS origin

HIV is thought to have originated in non-human primates in sub-Saharan Africa and transferred to humans during the 20th century. The epidemic officially began on 5 June 1981.[106]

Two species of HIV infect humans: HIV-1 and HIV-2. Both species of the virus are believed to have originated in West-Central Africa and jumped species (zoonosis) from a non-human primate to humans.

HIV-1 is thought to have originated in southern Cameroon after jumping from wild chimpanzees (Pan troglodytes troglodytes) to humans during the twentieth century.[107][108] It evolved from a Simian Immunodeficiency Virus (SIVcpz)[109]

HIV-2, on the other hand, may have originated from the Sooty Mangabey (Cercocebus atys), an Old World monkey of Guinea-Bissau, Gabon, and Cameroon.[15]

Early history
See History of known cases and spread for early cases of HIV / AIDS

AIDS denialism

Main article: AIDS denialism

Individuals, including several scientists who are not recognized experts on HIV, question the connection between HIV and AIDS,[110] the existence of HIV itself,[111] or the validity of current testing and treatment methods. These claims have been examined and rejected as having no validity,[112] although they have had a political impact, particularly in South Africa, where governmental acceptance of AIDS denialism has been blamed for an ineffective response to that country’s AIDS epidemic.[113][114][115]

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HIV vaccine research hits impasse

Posted by pozlife on May 23, 2008


By Helen Briggs
Science reporter, BBC News, Boston

HIV binds to the surface of the human immune (CD4) cell (PRNewswire dated 19/11/07)

HIV has evolved to protect itself from the human immune system

Scientists are no further forward in developing a vaccine against HIV after more than 20 years of research, a Nobel Prize-winning biologist has said.

Professor David Baltimore, president of the American Association for the Advancement of Science (AAAS), said there was little hope among scientists.

But he said that they were continuing efforts to develop a vaccine.

“Our lack of success may be understandable but it is not acceptable,” he said.

“Some years ago I came to the conclusion that our community had to seriously undertake new approaches or we might find ourselves with a worldwide epidemic and no effective response,” Prof Baltimore told the annual meeting of the AAAS in Boston.

“That is just where we are today.”

I believe that HIV has found ways to totally fool the immune system – so we have to do one better than nature

Professor David Baltimore

Is HIV beating the scientists?

HIV had evolved a way to protect itself from the human immune system, he said.

“This is a huge challenge because to control HIV immunologically the scientific community has to beat out nature, do something that nature, with its advantage of four billion years of evolution, has not been able to do,” Prof Baltimore said.

“I believe that HIV has found ways to totally fool the immune system.

“So we have to do one better than nature.”

‘One shot’

Attempts to control the virus through antibodies or by boosting the body’s immune system have ended in failure.

This has left the vaccine community depressed because they can see no hopeful way of success, Prof Baltimore said.

Cell virus

Guide: The biology of Aids

Among the novel techniques that scientists are turning to are gene and stem cell therapy, although these are still in their infancy.

“In the human you really only have one shot which is to try to change genes in stem cells,” said Prof Baltimore, one of the leading experts on the HIV virus.

“So we’re trying to do that, to design vectors that can carry genes that will be of therapeutic advantage.”

Prof Baltimore won the Nobel Prize in Medicine in 1975 for the co-discovery of reverse transcriptase, an enzyme that was later found to be used by HIV to replicate in human cells.

He now leads the Baltimore laboratory at Caltech, with support from the Gates Foundation, to look for ways to genetically boost the immune system against infectious agents, particularly HIV.

Pie chart

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Looking for love?

Posted by pozlife on May 23, 2008


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