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HIV hides within certain types of
cells and reproduces slowly, eventually causing chronic inflammation regardless
of drug treatment. According to Servio H. Ramirez PhD, assistant professor of
pathology and laboratory medicine at Temple University School of Medicine
(TUSM), although antiretroviral drugs allowed persons with HIV infection to
live longer, the patients continue to have extended exposure to low levels of
HIV replication and associated inflammation. It is believed that this
inflammatory process in the central nervous system (CNS) is the underlying
cause of HIV-associated neurocognitive disorder.
Researchers at TUSM’s Department of
Pathology and Laboratory Medicine and Center for Substance Abuse Research
investigated the connection between inflammation and neurocognitive conditions
linked to long-term HIV exposure. Ramirez and colleagues focused on the CB2
receptor, a protein located on the surface of macrophages. Macrophages are a
type of white blood cell that engulfs and destroys foreign agents, and the
researchers believed they are likely the primary reservoir for HIV. They are
the first cells infected after sexual transmission of the virus, are found in
every organ of the human body, and circulate in the blood. They believe that
macrophages may be carrying HIV into the brain, and initiating HIV-associated
cognitive decline.
CB2 is a binding site for
cannabinoids, active compounds of cannabis (marijuana), but does not transmit
the psychoactive effects of cannabis. The researchers hypothesized that CB2 may
play a role in blocking inflammation in the CNS. They discovered that synthetic
anti-inflammatory substances distantly related to the active ingredient in
marijuana may take the strength out of HIV while the virus is hiding in
macrophages. The researchers conducted experiments using a non-clinical HIV
macrophage cell model. They treated the HIV-infected cells with one of three
different synthetic CB2-activating compounds and sampled the cells periodically
to measure the activity of the enzyme called reverse transcriptase, which is
essential for HIV replication. After seven days, all three compounds had
successfully attenuated HIV replication.
Results suggest that selective CB2
agonists could potentially be used along with antiretroviral drugs to create
new HIV/AIDS drug treatments and that the human immune system could be enhanced
to fight HIV. Yuri Persidsky, MD, PhD, chair of TUSM’s Department of Pathology
and Laboratory Medicine and one of the researchers, commented that the study
suggests that stimulating CB2 receptors in white blood cells could produce
benefits against other viral infections.
The full article, “Attenuation of
HIV-1 Replication in Macrophages by Cannabinoid Receptor 2 Agonists,” was
published in the Journal of Leukocyte Biology (2013; 93 (5):801–810).
The Friends of AIDS Foundation is
dedicated to enhancing the quality of life for HIV positive individuals and
empowering people to make healthy choices to prevent the spread of the HIV
virus. To learn more about The Friends of AIDS Foundation, please visit: http://www.friendsofaids.org.
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