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Sleep Deprivation Contributes to Immune Activation in People With HIV Control
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CROI 2024 (Conference on Retroviruses and Opportunistic Infections), March 3-6, 2024, Denver
Mark Mascolini
Sleep deprivation tracked in a sleep lab led to a significant increase in CD8 T-cell activation and trends toward more monocyte and macrophage activation, according to results of a 20-person study [1]. Bernard Macatangay (University of Pittsburgh) and colleagues found no evidence of ectoenzyme expression that can counteract this deprivation-induced inflammatory processes in people with antiretroviral-controlled HIV infection.
Macatangay and collaborators noted that up to 70% of people with HIV complain of disturbed or insufficient sleep. Research shows that insomnia inflates risk of cardiovascular disease in people with HIV, and shortened sleep portends greater all-cause mortality in the general population. Because little is known about the impact of sleep duration on inflammation in people with HIV, Macatangay and coworkers conducted this study.
Extracellular adenosine limits tissue damage from inflammation while also mediating the sleep drive. Metabolism of this regulatory nucleoside gets upset in people with HIV, whose sleep behaviors can unsettle adenosine metabolism. The University of Pittsburgh team considered adenosine levels as a key to unlocking the mystery of how sleep deprivation affects inflammation in people with HIV.
The study involved 20 people with HIV infection, 75% of them men, and 35% African American. Median age stood at 59.7 and median CD4 count at 760. All participants controlled HIV with antiretroviral therapy. After 1 week of regularized sleep in which people could sleep 8 hours every night, participants stayed awake for 24 hours. The researchers sampled blood to measure key biomarkers before and after this sleep disturbance.
Acute sleep deprivation led to a significant increase in CD8-cell activation, signaled by percentage of CD38+ HLA-DR CD8s (P = 0.0281) but not CD4-cell activation. The researchers charted trends toward higher levels of IL-6 monocytes (P = 0.0776), TNF-alpha monocytes (P = 0.0604), and sCD163 (P = 0.0827) but not of sCD14, TNF-alpha, or IL-6.
Pladma levels of adenosine were similar before and after acute sleep deprivation, and deprivation did not boost T-cell expression of CD39, CD73, or both. There was a trend toward lower percent flow-mediated dilation reactivity after sleep deprivation (P = 0.07). Sleep deprivation did not lead to compensatory changes that could offset inflammation-related damage, like increased ectoenzyme expression that can boost extracellular adenosine and counteract deprivation-induced inflammation.
The Pittsburgh team believes their findings underline the need to find interventions that ease sleep disturbances in people with HIV to quell HIV-induced inflammation.
Reference
1. Borker PV, Morris B, Roscher J, Swanger S, Patel SR, Macatangay BJC. Increased Immune Activation following acute sleep deprivation in people With HIV on ART. CROI 2024 (Conference on Retroviruses and Opportunistic Infections), March 3-6, 2024, Denver. Abstract 351.
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