Genetic Mutation May Provide Protection Against Initial HIV Infection But May Raise Risk of Developing Dementia Once Infected, Study Says
A genetic mutation may act as a "double-edged sword," providing some protection against initial HIV infection but causing people to develop dementia more rapidly once HIV infection has occurred, according to a study appearing in the Oct. 15 issue of the Proceedings of the National Academy of Sciences, the San Antonio Express-News/Washington Times reports. Researchers from the University of Texas Health Science Center, Audie Murphy VA Hospital and Wilford Hall Medical Center examined blood and tissue samples from 1,115 adults with HIV and 592 children exposed to the virus in utero to determine whether the presence of a mutated form of the MCP1 gene was present and how that gene affected their chances of contracting the virus and developing dementia. The MCP1 gene regularly produces a protein that signals the body to produce cells known as monocytes and macrophages to regulate the body's immune system. A mutated form of the gene causes the body to produce an excess amount of the protein. The excess protein initially helps the body ward off HIV infection, according to the study, which found that people with the gene were 50% less likely to become infected with HIV. However, once infection has occurred, the excess number of monocytes and macrophages can cause inflammation and tissue damage, particularly in the brain. The researchers found that people with the mutation had a "fourfold" risk of developing dementia once they became infected with HIV compared to people without the mutation. The presence of the mutation also "seems to encourage HIV to multiply," Dr. Sunil Ahuja, one of the study's directors, said.
Identifying People at Risk
According to Lynn Pulliam, a professor of medicine and laboratory medicine at the University of California-San Francisco, other genetic markers for dementia have been identified. "This new data, taken together with previously published information, may suggest a genetic 'risk factor' profile for AIDS dementia can be developed so that these patients can be offered additional therapy when available," she said. Ahuja said that the study results still must be confirmed and noted that, as of yet, there is no way to "shut down" the mutant gene. "We can't immediately translate this to clinical care," he said, but added that the information supplies "one more brick in the wall" to suggest how HIV infection leads to diseases such as dementia (Tumiel, San Antonio Express-News/Washington Times, 10/22).