In the early years of the AIDS epidemic, being infected with the virus that causes the disease was considered a virtual death sentence. But with the development of antiretroviral therapy, many with HIV are now living much longer. In fact, it is estimated that by 2015, about half of all HIV-positive individuals will be older than 50.
Yet those over 50 also progress to AIDS faster than adults in their 20s or 30s. And those in the younger age bracket even those responding well to antiretroviral therapy still exhibit illnesses and clinical conditions commonly associated with older people, such as certain cancers and liver diseases. For the most part, the reasons for this have remained a mystery.
But a UCLA AIDS Institute study published Jan. 26 in the online journal PLoS ONE suggests a partial explanation, showing that HIV causes a specific subset of CD4+ "helper" T-cells which play an important role in the body's response to infection to age rapidly, by as much as 20 to 30 years over a three-year period.
In the study, researchers witnessed a decline in CD4+ T-cell numbers and, most strikingly, found that in the surviving T-cells, the HIV virus caused rapid and drastic shortening of the ends of chromosomes, called telomeres, which protect the chromosomes and prevent them from fusing together, much like plastic tips keep shoelaces from unraveling. Telomeres become progressively shorter during natural cell division; when they become too short, cells do not function properly.
"Our findings have important implications for the health of both young and old HIV-1infected adults," said lead investigator Tammy M. Rickabaugh, an assistant research immunologist in the division of hematology and oncology at the David Geffen School of Medicine at UCLA. "They underscore the importance of developing new approaches to boost immune function to complement current treatments, which are exclusively directed against the virus."
|Contact: Enrique Rivero|
University of California - Los Angeles