After HIV infection, an accelerated aging process at the DNA level has been seen

After HIV infection, an accelerated aging process at the DNA level has been seen ...

Researchers at the University of California, Los Angeles (UCLA) and colleagues claim that a new HIV infection might shorten the lives of an individual by nearly five years if they were not infected. The research shows how HIV has an effect on aging in infected individuals, accelerating biological changes in the body associated with normal age within two to three years of infection.

In a paper titled, HIV accelerates aging at the time of the initial HIV infection, the authors publish their findings in the scientific journal iScience.

Despite a significant increase in life expectancy, there is mounting evidence that long-term treatment with human immunodeficiency virus (HIV) and antiretroviral therapy, even when clinically well-controlled, is associated with an earlier than expected onset of chronic ailments such as heart and kidney disease, frailty, and neurocognitive difficulties, according to the scientists.

Elizabeth Crabb Breen, a professor emerita at UCLA's Cousins Center for Psychoneuroimmunology and of psychiatry and biobehavioral sciences, believes that even in the early months and years of living with HIV, the virus has already set into motion an accelerated aging process at the DNA level. This highlights the critical importance of an early HIV diagnosis and an awareness of aging-related problems, as well as the importance of preventing HIV infection in the first place.

The researchers analyzed stored blood samples from 102 men who became HIV infected six months or less prior to their infection, and again two to three years after their infection. They compared them with matching samples from 102 non-infected men of the same age taken over the same time period.

The scientists investigated how HIV affects epigenetic DNA methylation. Five epigenetic measures of aging are identified as epigenetic clocks. The fifth measure evaluated the length of telomeres.

In the absence of highly effective antiretroviral therapy, HIV-infected individuals demonstrated significant age acceleration in each of the four epigenetic clock measurements ranging from 1.9 to 4.8 years, as well as telomere shortening over the time starting just before infection and ending two to three years after.

According to senior author Beth Jamieson, a professor in the Geffen School's hematology and oncology department, our access to rare, well-characterized samples allowed us to design this study in a way that leaves little doubt about the role of HIV in eliciting biological signatures of early aging. We hope to investigate whether an individual is at an increased risk for certain aging-related illness outcomes, thus identifying new therapeutic targets.

The researchers identified problems with the investigation.

This paper emphasizes the importance of recognizing how rapid the initial HIV infection begins accelerating epigenetic measures of aging, and provides a framework for further investigation of characterizing these epigenetic measures as predictors of future clinical outcomes and impacts on health spans.

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