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HIV accelerates development of age-related illnesses
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An increased risk for age-related illnesses among HIV patients may develop from epigenetic changes induced by the infection, according to recent data.
“While we were surprised by the number of epigenetic changes that were significantly associated with both aging and HIV infection, we were most surprised that the data suggests HIV infection can accelerate aging-related epigenetic changes by 13.7 to 14.7 years,” Beth D. Jamieson, PhD, of the David Geffen School of Medicine at UCLA, said in a press release. “This number is in line with both anecdotal and published data suggesting that treated HIV-infected adults can develop the diseases of aging mentioned above, approximately a decade earlier than their uninfected peers.”
Jamieson and colleagues examined white blood cells collected from two groups of men aged 20 years to 35 years, as well as two older cohorts of men aged 36 years to 56 years. Each group of 12 samples from men with HIV, who had not started ART, was age-matched with 12 samples from participants without the infection, resulting in 96 blood samples. From these, peripheral blood mononuclear cell samples were isolated and either stained for flow cytometry analysis or used for genomic DNA isolation and methylation level analysis.
The effects of age and HIV infection on methylation at CpG sites related to aging showed correlations of 0.49 (P < 1x10-200) and 0.47 (P < 1x10-200), respectively. When using these epigenetic patterns to estimate the age of the sample’s donor, the researchers found that those with HIV appeared to be aged approximately 14 years older than their true age.
“These data suggest that HIV-1 infection does accelerate some aspects of aging, and that general aging and HIV-1-related aging work through some common cellular and molecular mechanisms,” the researchers wrote. “These results are an important first step for finding potential therapeutic targets and novel clinical approaches to mitigate the detrimental effects of both HIV-1 infection and aging.”
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Paul A. Volberding, MD
The relationship between HIV and aging has been under intense review for the past several years. Many patients with HIV express the feeling that they seem older than they expect, and studies have shown that some (but not all) diseases associated with aging occur at earlier ages in persons with HIV compared with those without HIV. A constant issue in this question surrounds the definition of aging. How is it measured? How do you take into account other differences in the infected and uninfected populations? For example, cardiovascular disease is seen at earlier ages in patients with HIV, but this group also has a much higher smoking rate, itself a cardiovascular risk factor.
The current manuscript in PLoS One by Rickabaugh and colleagues injects fresh insights into this ongoing debate. These investigators, rather than compare age-associated morbidities, employ genomic markers of cellular aging to explore differences potentially caused by HIV infection. Their model of DNA methylation in a small cohort (12 infected, 12 uninfected) at younger (20 to 35 years) compared with older (35 to 56 years) men in the MACS cohort finds significant differences associated with HIV infection. Compared with controls without HIV, individuals with HIV had a methylation pattern associated with aging more than the uninfected group.
While quite interesting, some caution seems in order. The sample size in this report is very small. And the “older” group is still quite young. One might also ask whether this method is affected by other comorbidities and exposures and ultimately whether it can be shown linked to differences in clinical outcomes. Still, this is an intriguing observation that should keep the HIV and aging debate moving forward. Definitely worth close follow-up.
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