Success of HIV may depend in its mutations

by Medindia Content Team on  November 13, 2002 at 4:47 PM Research News
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Success of HIV may depend in its mutations
Researchers observe that one reason AIDS may progress as a disease is the human immunodeficiency virus mutates so rapidly within the human body that it confounds the already-weakened immune system's ability to defend against it. In addition, conventional tests used to determine how well a person infected with HIV can mount an immune defense can be misleading, the researchers, from Harvard Medical School's Center for Blood Research, have found.

"The immune system needs to evolve along with the virus and this evolution becomes difficult because it is in a milieu of immune deficiency," researcher Premlata Shankar told United Press International. We overstate the immune response because the virus used to test a person's response has many regions to which an immune response has already been developed.

As reported in the November issue of the Journal of Clinical Investigation, although the immune system's memory-based component might continue to resist the strain of HIV it first encountered -- or strains used in laboratory tests -- subsequent viral mutations weaken its ability to mount an effective defense.

Although HIV's ability to mutate rapidly has been well documented, the effects of those mutations on an infected individual have not been studied thoroughly. So Shankar and colleagues examined the immune system's killer cell responses to mutated forms of HIV taken from infected people at different stages of their infection. They found the killer cells from patients with more advanced infections could not destroy the mutated virus, even though they still could neutralize common laboratory strains.

In contrast, killer cells from people with less-advanced HIV infections could destroy both the lab test strains and their own mutated forms. "The side-by-side comparison of cellular responses to laboratory strains and autologous (mutated after infection) strains at different disease stages is new," immunologist Beth Jamieson, with the David Geffen School of Medicine at the University of California, Los Angeles, told UPI. "This shows that the response to virus is lost later in infection. Now we need to know why," she said. "While there are no direct implications for diagnosis or treatment, an important motivation for this sort of study is the development of knowledge that could lead to successful HIV vaccines, both to prevent and to treat HIV infection," infectious disease specialist Stuart Ray, of the Johns Hopkins University School of Medicine in Baltimore, told UPI. When a person is first infected with HIV, his or her immune system responds by producing killer T-cells, called CD8- T, and CD4-T helper cells. The system also remembers the type of molecules on the surface of the attacking virus, so the next time the system encounters the virus, it produces many cells from memory to attack it again. But when the virus mutates, the immune system is no longer able to identify and kill the mutations.

The researchers found much of the deficiency also occurs because HIV destroys the helper cells. This stops the efficient production of new killer cells and it helps to weaken the killer cells that are produced. Because of this finding, Jamieson recommended further research "looking at the epitopes (surface proteins) on the virus over time in individuals."


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