Toward the end of the last decade, scientists at the National Institutes of Health (NIH) made one of the most important discoveries regarding HIV: that the virus uses receptors other than CD4 to enter and infect T-cells. These coreceptors function somewhat like doorknobs, and HIV must first bind and attach to CD4, and then to one of two other coreceptors, either CCR5 or CXCR4, to enter cells.
After detecting these coreceptors, researchers made several other key discoveries. First, they found that people whose virus prefers to use CXCR4 tended to have lower CD4 counts and faster HIV disease progression than people whose virus prefers CCR5. Second, they found that those born without the ability to make the CCR5 coreceptor were highly resistant to HIV infection. This led to the development and approval of a drug to block CCR5, that drug being Selzentry. For Selzentry to work, however, a person must only carry CCR5-tropic virus and not CXCR4-tropic or mixed-tropic virus.
The participants in both groups were similar in most respects, and overall the study found that the two different regimens had similar efficacy. Seclén’s group, however, was interested not in how those treatments compared with one another, but in how a person’s HIV tropism would affect his or her response to starting either treatment.
Of the 482 participants in the study who were treated for at least 48 weeks, 14 percent had CXCR4-tropic virus at the start of the study. The rest had CCR5-tropic virus. Also, 22 percent had a strain of HIV (called a clade) other than clade B, the most common strain in Western Europe and the United States.
Seclén and his colleagues found that a person’s tropism significantly affected the response to treatment. Overall, while 92 percent of those with CCR5-tropic virus had an undetectable viral load after 48 weeks of treatment, this was true in only 77 percent of those with CXCR4-tropic virus. When multiple factors were considered, a person’s tropism remained significant until the 24-week point. In people with clade B virus, however, tropism was significant at both 24 and 48 weeks. Contrary to other studies, those with CXCR4-tropic virus had similar increases in CD4 counts as those with CCR5-tropic virus.
“In antiretroviral-naïve patients beginning antiretroviral therapy, baseline…tropism seems to be an independent predictor of virologic response,” conclude the authors, adding that “this observation may have important clinical implications for the monitoring of antiretroviral therapy and interpretation of comparative trials.”
ENDS
More on Tropism and drugs prescriptions HERE
Your doctor needs to know your HIV tropism before prescribing co-receptor antagonists. Your HIV has its own unique identity. Tropism refers to the co-receptor that a particular HIV strain uses to enter the CD4+ cell. The two most common co-receptors are CCR5 (R5) and CXCR4 (X4). Trofile™ is a novel test that pinpoints your tropism status –R5, X4, or a combination of these known as dual/mixed. Trofile reveals if your virus primarily uses the CCR5 co-receptor. This can help your doctor decide to prescribe a CCR5 antagonist. This new class of antiretrovirals targets CCR5-specific HIV entry into the cell.
How does tropism affect my treatment plan?
If your HIV tropism is CCR5, there’s a new kind of medicine that can help stop HIV from getting in.
Peace and tolerance
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