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HIV infection accelerates biological aging
Epigenetic aging accelerates and telomeres shorten 2-3 times faster in HIV-infected subjects.
The human immunodeficiency virus (HIV) has negative implications extending beyond its impact on the immune system. Research shows that long-term infection with HIV coupled with the use of antiretroviral therapy is linked to a faster onset of chronic disorders. Examples of the latter include heart diseases, kidney disorders, frailty, and neurocognitive conditions. This suggests that HIV infection could potentially accelerate the aging process.
Epigenetic clocks and telomere length have been used as tools to assess biological aging. In the context of HIV, using these tools has been limited to cross-sectional studies comparing individuals with established or chronic HIV to age-matched healthy counterparts. However, longitudinal studies examining accelerated aging in the same individual across the spectrum of HIV infection are lacking.
To address the abovementioned gap, Breen et al. initiated the first of its kind (according to the investigators' knowledge) longitudinal study. It aimed to assess the impact of HIV infection on epigenetic age, using several DNA methylation-based measures. The study followed 204 male participants (where 102 had persistent HIV-negative results and 102 who became HIV infected) before and three years after infection with HIV. They hypothesized that HIV viral load significantly contributes to early accelerated epigenetic aging.
Results revealed that before HIV infection, the difference between chronological age and epigenetic age between subjects was insignificant. After HIV infection, those with the virus had accelerated epigenetic aging and telomere shortening compared to non-infected participants. Also, infected individuals had accelerated epigenetic aging and telomere shortening compared to themselves before becoming HIV positive. The latter was not the case in non-infected individuals. Further analysis revealed that epigenetic aging accelerates and telomeres shorten 2-3 times faster in HIV-infected subjects.
The researchers concluded that HIV infection significantly impacts aging, where initial infection accelerates epigenetic aging. This lays the foundation for further investigation to utilize epigenetic measures as predictors of healthspan and clinical outcomes.
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The human immunodeficiency virus (HIV) has negative implications extending beyond its impact on the immune system. Research shows that long-term infection with HIV coupled with the use of antiretroviral therapy is linked to a faster onset of chronic disorders. Examples of the latter include heart diseases, kidney disorders, frailty, and neurocognitive conditions. This suggests that HIV infection could potentially accelerate the aging process.
Epigenetic clocks and telomere length have been used as tools to assess biological aging. In the context of HIV, using these tools has been limited to cross-sectional studies comparing individuals with established or chronic HIV to age-matched healthy counterparts. However, longitudinal studies examining accelerated aging in the same individual across the spectrum of HIV infection are lacking.
To address the abovementioned gap, Breen et al. initiated the first of its kind (according to the investigators' knowledge) longitudinal study. It aimed to assess the impact of HIV infection on epigenetic age, using several DNA methylation-based measures. The study followed 204 male participants (where 102 had persistent HIV-negative results and 102 who became HIV infected) before and three years after infection with HIV. They hypothesized that HIV viral load significantly contributes to early accelerated epigenetic aging.
Results revealed that before HIV infection, the difference between chronological age and epigenetic age between subjects was insignificant. After HIV infection, those with the virus had accelerated epigenetic aging and telomere shortening compared to non-infected participants. Also, infected individuals had accelerated epigenetic aging and telomere shortening compared to themselves before becoming HIV positive. The latter was not the case in non-infected individuals. Further analysis revealed that epigenetic aging accelerates and telomeres shorten 2-3 times faster in HIV-infected subjects.
The researchers concluded that HIV infection significantly impacts aging, where initial infection accelerates epigenetic aging. This lays the foundation for further investigation to utilize epigenetic measures as predictors of healthspan and clinical outcomes.
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
Quality Garant
Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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