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Sexual Minority Stress and Accelerated Cellular aging in Treated HIV Infection
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IAS 2021 July 18-22
D. Ghanooni • (1), A. Carrico (1), R. Williams (1), T. Glynn (2), J. Moskowitz (3), S. Dilworth (1), S. Pahwa (4), D. Fuchs (5), B. Aouizerat (6), A. Flentje (7)
(1) University of Miami, Public Health Sciences, Miami, United States, (2) University of Miami, Psychology, Coral Gables, United States, (3) Northwestern University, Medical Social Sciences, Chicago, United States, (4) University of Miami, Microbiology and Immunology, Miami, United States, (5) Innsbruck Medical University, Innsbruck, Austria, (6) New York University, College of Dentistry, New York City, United States, (7) University of California, School of Nursing, San Francisco, United States
Abstract:
BACKGROUND: Gay, bisexual, and other men who have sex with men experience stigma related to their sexual minority status that is theorized to drive negative health outcomes. Among people living with HIV, even those who achieve an undetectable viral load display immune dysregulation, which could be amplified by sexual minority stress to accelerate cellular aging.
METHODS: This cross-sectional study enrolled 51 methamphetamine-using sexual minority men with an undetectable viral load. Participants completed measures assessing sexual minority stress, negative attitudes towards being a sexual minority (i.e., internalized heterosexism), and degree of openness about one's sexual minority status (i.e., outness). The epigenetic clock, a validated measure indexing methylation of specific CpG sites, and leukocyte telomere length were estimated using genome wide DNA methylation. Soluble markers of immune activation (e.g., sCD14) and inflammation (e.g., TNF-aRII) were measured in plasma.
RESULTS: Participants were on average 43 years old (SD= 9), non-Hispanic White (51%), exclusively gay (76%), and had been diagnosed with HIV for an average of 14 years (SD= 9). As shown in the Figure, sexual minority stress was associated with a faster epigenetic clock. Even after adjusting for negative affect and recent stimulant use, greater sexual minority stress was independently associated with a faster epigenetic clock (i2 = 0.33, p &It;= 0.018) and shorter estimated leukocyte telomere length (i2 = -0.48, p = 0.001 ). Although greater internalized heterosexism (r = -0.31, p &It; = 0.029) and decreased outness (r = 0.28, p = 0.046) were associated with shorter leukocyte telomere length, these associations were not statistically significant in adjusted models. Soluble markers of immune activation and inflammation were not significantly associated with methylation¬derived measures of cellular aging.
CONCLUSIONS: Longitudinal research is needed to elucidate the bio-behavioral mechanisms linking sexual minority stress processes with accelerated cellular aging in sexual minority men with and without HIV.
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