Commentary from the CDC HIV/STD/TB Prevention News Update 05/02/02:
Scientists who study the immune systems of HIV patients have confirmed a long-standing suspicion: The deadly virus targets the very cells programmed to attack it. The findings could help in the design of effective HIV vaccines, and also raise a caution about "drug holidays," in which HIV patients are temporarily taken off intensive drug therapy in the hopes of boosting their natural immune response to the virus. When the scientists studied four HIV patients who were temporarily taken off drug therapy as part of a clinical trial, they found that their HIV levels rose significantly. That spurred a corresponding surge in HIV-specific CD4 cells, which, in turn, gave the virus more potential targets.
"This is a sobering paper because it tells us that we have a difficult task ahead if we're going to overcome this virus," said Dr. Anthony Fauci, chief of infectious diseases for the National Institutes of Health (NIH). A team of NIH researchers studied CD4 T cells in the blood of 12 HIV-positive people. They found that the CD4 cells that specifically target HIV contained two to five times more HIV than the other cells, a finding that supports the presumption that HIV selectively infects the cells that attack the virus.
The findings, appearing in today's issue of the journal Nature (2002;417:95-98), could have implications for efforts to produce an HIV vaccine, said the study's lead investigator, Daniel Douek of the NIH's National Institute of Allergy and Infectious Diseases. That's because the same infection-fighting cells that a vaccine would send into action in the face of HIV - the HIV-specific CD4 cells - would only provide the virus with the most attractive targets to infect. Douek said the findings suggest that a more effective vaccine would elicit a strong response of both the HIV-specific CD4 cells and the body's CD8 white blood cells - killer cells not infected by HIV - while also rallying anti-HIV antibodies.
(CDC HIV/STD/TB Prevention News Update 05/02/02)
