POZlife

POZLife: Life from the Infected and Effected point of veiw.

Crystal Risk: Meth Increases Immune System Receptor for HIV Infection

Posted by pozlife on August 7, 2006

 

 

 

A
new study has demonstrated that methamphetamine stimulates production
of a receptor on immune system cells, potentially increasing the risk
of HIV infection. The research, conducted at the University of Buffalo,
is the first to demonstrate that meth can cause biological changes that
render users of this illicit drug more susceptible to infection if they
are exposed to the virus.

 

 

 

Methamphetamine, often
referred to as “crystal” or “tina,” is a highly addictive stimulant. It
has found a wide audience among suburban teens, students,
professionals, and homemakers who work long hours. Of particular
concern has been the reported widespread use of the drug among men who
have sex with men.

 

 

 

Various studies have documented
that, when meth is used in association with sexual activity, condoms
are more likely to be abandoned and the number of sex partners are more
likely to increase. These behavioral factors have been repeatedly shown
to increase the risk of exposure to HIV.

 

 

 

The new study, to be published in the September issue of the Journal of Neuroimmune Pharmacology,
suggests that not only is meth use associated with risky behavioral
factors, it may also render certain immune system cells more likely to
pick up HIV, present the virus to T-cells, and jumpstart the infection
process.

 

 

 

“This finding shows that using meth is doubly
dangerous,” said Madhavan Nair, PhD, Professor of Medicine at the
University of Buffalo and a lead investigator of the study.

 

 

 

The
new research involves dendritic cells, which serve as the first line of
defense against disease-causing pathogens that come into contact with
mucosal tissues in the body, such as those inside the anus. These cells
produce receptors, including binding receptors used by HIV (DC-SIGN)
and dopamine receptors.

 

 

 

Dr. Nair’s group has
demonstrated that meth’s stimulation of dendritic cells via the
dopamine receptors consequently increases the production of DC-SIGN. In
turn, dendritic cells can become overloaded with HIV and overwhelm
T-cells, essentially aiding the HIV infection process along. In fact,
Dr. Nair and his colleagues have demonstrated that meth can affect a
variety of dendritic cell functions that are necessary to augment a
healthy immune response to a variety of disease-causing pathogens.

 

 

 

“Now
that we have identified the target receptor, we can develop ways to
block that receptor and decrease the viral spread,” said Dr. Nair. “If
we could prevent the upregulation of the meth-specific dopamine
receptor by blocking it, we may be able to prevent the interaction of
meth with its specific receptors, thereby inhibiting the virus
attachment receptor. [This] could be beneficial therapeutically to
reduce HIV infection in these high-risk populations.”

 

 

 

Source:

 

 

 

University of Buffalo

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