HIV Ages Critically-Important Immune Cells

Scientists from the United States announce that they managed to discover one of the main mechanisms through which the human immunodeficiency virus (HIV) acts on the human immune system, weakening it, and making it incapable of fighting future infections.

The team found out that the viral agent was causing a specific subset of CD4+ “helper” T cells in the immune system to become older at a very fast pace – 20 to 30 years in just over three years.

According to the group, this finding may go a long way towards explaining why children and teenagers who are very young tend to develop conditions associated with old age after HIV infections.

Most commonly, they start suffering from a variety of forms of cancer, and also from liver diseases. Researchers at the University of California in Los Angeles (UCLA) believe that this is caused by the aging of immune cells, which is brought on by the virus.

Over the past few years, researchers managed to create successful antiretroviral therapies, that help extend patients' lives until the age of 50 and beyond. People who are older than that experience a very accelerated evolution in their condition.

But HIV patients in their early 20s, or even younger, are at risk of succumbing from diseases usually related to senior years. Experts say that the decline in CD4+ T-cell numbers is to blame for this.

Details of the new study, which was conducted by experts at the UCLA AIDS Institute, appear in the latest online issue of the open-access, peer-review scientific journal PLoS ONE, a publication of the Public Library of Science.

“Our findings have important implications for the health of both young and old HIV-1–infected adults,” says UCLA David Geffen School of Medicine expert Tammy M. Rickabaugh.

She was also the lead investigator of the new research. The scientist holds an appointment as an assistant research immunologist in the School's Division of Hematology and Oncology.

“They underscore the importance of developing new approaches to boost immune function to complement current treatments, which are exclusively directed against the virus,” adds Rickabaugh.

In the experiments, it was determined that CD4+ T cell numbers decreased following HIV infection. It was also found that the viral agent tended to shorten the telomeres on the end of each chromosome in the immune cells.

Telomeres play a role in protecting the chromosomes, and preventing them from fusing together. When these structures are too short, cells no longer function properly, and may become cancerous.

"Taken together, our results help to explain some of the clinical observations that have been documented in HIV-infected people and emphasize the need for developing therapeutic approaches directed at improving the naive immune cell compartment,” Beth D. Jamieson explains.

“This is critically important in light of the demographic shift of HIV-infected persons,” explains the UCLA David Geffen School of Medicine senior study investigator.

The expert holds an appointment as an associate professor of medicine in the Division of Hematology and Oncology at the university.

The new study was conducted with funds from the National Institute of Allergy and Infectious Diseases, the National Institute on Aging, the National Cancer Institute, the National Heart, Lung and Blood Institute, and the UCLA Jonsson Comprehensive Cancer Center.

The UCLA AIDS Institute and the David Geffen School of Medicine also supported the work in part.