Patients diagnosed with AIDS, a virtual death sentence, apparently benefit from antiretroviral therapy. Novel developments in this therapy can probably improve the survival rate of AIDS patients. A groundbreaking research undertaken by the UCLA scientists recently noticed that HIV virus triggers rapid and drastic shortening of the ends of chromosomes, termed as telomeres, along with a decline in the number of CD4+ T-cells. These telomere ends are believed to guard the chromosomes and restrict them from fusing together.
HIV supposedly empowers specific subset of CD4+ ‘helper’ T-cells to interfere with the body’s response towards infection and age in a period of three years. As the telomeres shorten during natural cell division, they become too short and make cells incapable of performing functions appropriately. In the current investigation, researchers evaluated two subsets of CD4+ T-cells (CD45RA+ CD31+ and CD45RA+ CD31-) in two groups of individuals aged 20–32 and 39–58 years. All the participants were suffering from HIV for one to three years and were not treated with antiretroviral therapy. Both the groups were compared with samples from age-matched controls who were HIV seronegative.
“Our findings have important implications for the health of both young and old HIV-1–infected adults,” elucidated, 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.”
Throughout the research, experts focused on ‘naive’ T-cells which apparently underwent unexpected rapid aging due to HIV-1. This speed of aging is probably equal to 20 to 30 years of aging within three years of infection. The number of CD31- T-cells seemingly fighting against new pathogens also declined remarkably. Investigators examined HIV-positive individuals subjected to antiretroviral therapy for two years and whose therapy had successfully kept HIV-1 under control. The therapy presumably kept their viral loads at undetectable levels, but failed to restore the immune system completely. Hence, younger HIV-positive people may tend to become ill with conditions more common to older people. The research findings call for the need to develop therapeutic approaches directed at boosting the naive immune cell compartment.
The research is published in the online journal PLoS ONE.