Even with PrEP and the growing number of antiretrovirals, the HIV/AIDS crisis hasn’t gone anywhere.  Instead, the epidemic continues to loom over us.

And here’s alarming news to take note of: researchers at the University of California (UCLA) report in the news source iScience that within the first few years of becoming infected with HIV, the virus significantly speeds up aging at the cellular level. These findings underscore the importance of early diagnosis and speedy treatment of HIV.

The UCLA research team observed that during the first two to three years after infection, the DNA of HIV-positive men showed evidence of aging up to five years faster than a comparable group of men who remained HIV negative.  The team concluded that initial HIV infection is associated with significant changes in genomic (DNA) aging, which may explain why people living with HIV experience aging-related illnesses earlier.

According to Poz.com, “Over half of people living with HIV in the United States are over age 50. People aging with HIV face some unique challenges, even with treatment that lets them live longer, healthier lives. They are more likely to deal with coexisting conditions, like heart disease, kidney problems, frailty and cognitive decline, in addition to increased social and mental health concerns.”

During the study, UCLA scientists compared biomarkers of the cellular aging process over time in blood samples from 102 men who were diagnosed with HIV and an equal number who remained HIV negative.  As a result, the researchers were able to measure cellular aging in samples collected six months or less before the men acquired the virus and again two to three years later.

The males were participants in the Multicenter AIDS Cohort Study, a comprehensive study of MSM (men who have sex with men) that includes regular blood draws, physical exams, and mental health questionnaires. They were mostly white and college-educated with an average age of 39. Most acquired the virus before 1995, and none were on effective antiretroviral therapy when the second blood sample was collected. All the men started with a median CD4 T-cell count of around 1,000, but this fell to approximately 600 for those who acquired HIV.  The researchers claim to be the first to track cellular aging at this scale throughout initial infection in HIV-positive persons.

“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,” stated senior author Beth Jamieson, Ph.D., a professor at the David Geffen School of Medicine.  “Our long-term goal is to determine whether we can use any of these signatures to predict whether an individual is at increased risk for specific aging-related disease outcomes, thus exposing new targets for intervention therapeutics.”

According to Poz.com, the focus of the study was epigenetic signs of aging, that is to say, which genes are turned on and off at different points in time. “Four different epigenetic ‘clock’ metrics based on DNA methylation, which determines gene expression, were used to evaluate how old someone’s genes looked compared to how they should look at a given age. These clocks are derived from hundreds of sites on the human genome.”

Before initial HIV infection, the males in both groups had epigenetic ages that matched their actual chronological ages within a year without any consequential differences between them.  However, at the following visit, the men who contracted HIV showed significant aging according to three of the four epigenetic clock measures compared with those who remained HIV negative. Acceleration varied across the clocks: One showed a median of 1.9 years of accelerated aging, while two others showed a median of 4.8 years.

The authors of the study also measured telomere length, one of the best-known genetic indicators of aging. Telomeres are caps on the ends of chromosomes that seal the DNA strands, like the plastic tips on shoelaces. Over time, telomeres progressively shorten as cells divide.

The research uncovered that telomeres were significantly shorter in people who acquired HIV than would otherwise be expected.  According to the Centers for Disease Control and Prevention (CDC), other factors–such as smoking, poor diet, and psychological stress–can also shorten the telomeres.

“Prior studies have also seen an association between HIV and expedited telomere shortening,” stated Poz.com. “In 2020, another UCLA team found that antiretroviral treatment can slow but not stop the virus’s impact on cell aging. Initial HIV infection explained the jolt in cellular aging even after demographics, health status and risk factors were taken into account, according to researchers.” These additional factors included body mass index, hepatitis B, smoking, and T-cell counts.

The researchers concluded, “These longitudinal observations clearly demonstrate an early and substantial impact of HIV infection on the epigenetic aging process and suggest a role for HIV itself in the earlier onset of clinical aging.”

What’s important to keep in mind is that although the current study is the largest of its type, each group still consisted of just more than a hundred people. All participants were men, and most were Caucasian; therefore, the patterns might not be the same for women or people of color. In addition, since the HIV-positive men were not yet on effective treatment, the researchers could not consider the effects of antiretroviral therapy.

“Our work demonstrates 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,” stated Elizabeth Crabb Breen, Ph.D., professor emerita at UCLA’s Cousins Center for Psychoneuroimmunology.  “This emphasizes the critical importance of early HIV diagnosis and an awareness of aging-related problems as well as the value of preventing HIV infection in the first place.”