Treatment News : Study Suggests HIV Causes Rapid Aging of Key Immune Cells

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January 28, 2011

Study Suggests HIV Causes Rapid Aging of Key Immune Cells

A new study by researchers at the University of California at Los Angeles (UCLA) suggests that HIV causes immune cells to age quicker than normal—potentially causing more rapid HIV disease progression in older people with HIV and earlier onset of aging-related diseases in younger people. These data were published January 26 in the online journal PLoS One.

Experts have noted for some time that people older than 50 tend to have faster disease progression and poorer immune recovery when they become infected with HIV than people who become infected at a younger age. Moreover, evidence is mounting that a host of diseases that typically strike the elderly—such as cardiovascular disease and certain cancers—are occurring at much higher rates in people with HIV and at a younger age. All of this has led scientists to question whether HIV might be leading to accelerated aging.

One theory to explain at least some of these phenomena is accelerated aging of immune system cells in people with HIV, a condition called “immune senescence.” When people get older, and their cells have reproduced for many generations, the tips of their mitochondrial DNA—a snippet of the DNA called telomeres—become shorter and more ragged, much like the worn caps at the ends of used shoelaces. When telomeres degrade like this, the cells don’t function or reproduce well. This can cause the body to destroy those cells. It can also lead those cells to become cancerous.

To further illuminate what is happening with telomeres in HIV-positive people, Tammy Rickabaugh, PhD, and Beth Jamieson, PhD, from UCLA, and their colleagues looked at the effect of telomere length on people’s ability to produce and preserve naive CD4 cells—cells that had not previously encountered any pathogens and thus act as a reserve against future infections and cancers.

Rickabaugh’s team looked at the telomeres of four groups of people: One group consisted of HIV-negative people ages 19 to 30; one group consisted of HIV-positive people ages 20 to 32; and a third group included HIV-positive people ages 39 to 58. A fourth group was culled from a separate study and consisted of people with HIV who had been on ARV treatment for two years and whose therapy had successfully kept their HIV under control.

The team found that in the two groups of younger people, the HIV-positive group had much shorter telomeres than the HIV-negative group. In fact, the HIV-positive participants’ telomeres were as short as that typically found in people who are 20 to 30 years older.

In the older participants, Rickabaugh and her colleagues found that shorter telomeres were associated with low numbers of the type of immune cells needed to mount and sustain an adequate response to HIV and other diseases. The authors suggest this could explain why people who become infected at an older age have a quicker progression to AIDS, in the absence of treatment, and also why they tend to have poorer recovery of CD4 cells after starting ARV therapy.

What’s more, when Rickabaugh’s team looked at the group responding well to ARV therapy, they found that telomeres were shorter within just a few years of infection and that while naive cells did recover somewhat after starting treatment, they did not do so completely and remained impaired.

The authors acknowledge that while their study had different findings compared with those of some other studies, they believe their methods were more rigorous than those employed by other researchers, both in terms of the types of naive cells they investigated and because the two groups of younger participants were matched in age.

“Our findings have important implications for the health of both young and old HIV-infected adults,” Rickabaugh said. “They underscore the importance of developing new approaches to boost immune function to complement current treatments, which are exclusively directed against the virus.”

Search: telomeres, immune senescence, naive CD4 cells, aging, rapid aging, cardiovascular disease, cancer, Tammy Rickabaugh, Beth Jamieson

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