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  11th IAS Conference on HIV Science 18-21 July 2021
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Stress & Aging, Sleep & Brain
  - these studies reflect why mental health affects physical health & life expectancy.
social determinants of health contribute to aging & Comorbidities disease in HIV. Mental health is a contributor to physical health yet gets little attention. Viral suppression is the main focus of HIV care while this other aspect has been relatively ignored. Now with our aging HIV community the affects of mental health & stress are becoming more important & beginning to get more attention because aging has become a more important issue & getting more attention. With the discussion around that “patient-centered” care is increasing important for the aging & elderly population much more attention must be paid to mental health & social determinants of all the different communities with HIV. Its not enough anymore to only aim for viral suppression & to treat a Comorbidities condition. Clinics & care must address concretely mental health. here are 3 selected studies of importance at IAS, and a link below to a full report on comorbidities, aging & metabolics studies at IAS. Plus, research must focus more on these issues to understand their impact on health & longevity & QOL; as well, implementation studies ca be implemented to improve mental health, longevity & outcomes for elderly & aging PLWH. Jules Levin
IAS: Sexual Minority Stress and Accelerated Cellular aging in Treated HIV Infection - (08/06/21)
Sexual minority stress stems from the social stigma, prejudice, and discrimination that sexual minority persons experience. Informed by Meyer’s Minority Stress Theory, sexual minority stress processes are theorized to be important determinants of health disparities in sexual minority men. This is supported in part by findings that sexual minority stress and homophobic victimization are associated with elevated gene expression in sexual minority men living with and without HIV. We hypothesized that sexual minority stress responses could amplify key biological processes (e.g., inflammation) to accelerate epigenetic aging in sexual minority men living with treated HIV.
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. HIV infection is associated with immune system hyperactivation and shorter DNA telomere length. Even among those receiving effective ART who achieve and maintain undetectable viral load, residual immune dysregulation and inflammation could partially explain accelerated aging. Following ART initiation, methylation of cytosine - phosphate -guanine (CpG) groups related to accelerated cellular aging is attenuated, but epigenetic clock’s extrinsic epigenetic age acceleration (EEAA) remains elevated.
Participants were on average 43 years old (SD = 9), non-Hispanic White (51%), gay-identified (76%), and had been diagnosed with HIV for 14 years (SD = 9). After adjusting for negative affect and recent stimulant use, greater sexual minority stress was independently associated with a faster epigenetic clock (β = 0.33, p = 0.018), shorter telomere length (β = -0.48, p = 0.001), and fewer CD4+ (β = -0.56, p = 0.002) and CD8+ (β = -0.63, p < 0.001) naïve T-cells. Although greater internalized heterosexism and less outness were also associated with shorter telomere length and fewer naïve T-cells, these associations were no longer statistically significant in our adjusted analyses.
DISCUSSION: (1) Sexual minority stress was consistently and independently associated with methylation-derived estimates of accelerated cellular aging in sexual minority men living with treated HIV. (2) Findings highlight the potential relevance of sexual minority stress responses for accelerated aging in men living with treated HIV. (3) Results support the scientific premise of longitudinal research to identify the bio-behavioral pathways whereby sexual minority stress could potentiate accelerated aging. (4) Randomized controlled trials are needed to test the efficacy of psychological interventions targeting sexual minority stress processes for mitigating accelerated biological aging in men with treated HIV.
Psychological Stress & Brain, Inflammation & Stroke in PWH

In this cohort of PWH with well-controlled infection, we observed moderate associations between several measures of psychological stress and stress -responsive brain regions, including the amygdala and hippocampus.
Perceived and chronic stress were associated with carotid arterial inflammation.
These findings warrant further investigation into the mechanisms by which stress and brain metabolic activity in stress-responsive regions are associated with greater arterial inflammation in PWH.
Rates of stroke are higher in people living with HIV (PWH) than in people without HIV. Excess stroke risk in PWH may be attributed, in part, to traditional cardiovascular disease (CVD) risk factors and HIV-related variables. However, even after accounting for these factors, ischemic stroke risk remains up to 65% higher for PWH.
- Psychological stress, which is prevalent in PWH, is an established precipitant of inflammation and cerebrovascular disease in the general population and may be a novel contributor to stroke risk in PWH. We demonstrated in 293 individuals without HIV that stress and amygdalar network activity - a key driver of the neural inflammatory response to stress - are independently associated with arterial inflammation and strokes. Our central hypothesis is that stress contributes to stroke risk in HIV through activation of neural inflammatory pathways.
To test this, we examined the relationship between stress, metabolic activity in stress-related brain regions including in the amygdala network, and arterial inflammation on 18F-fluorodeoxyglucose (FDG)-PET, which is predictive of ischemic stroke and CVD events, in virally suppressed PWH.
(1) metabolic activity was significantly lower (p=0.005) in the bilateral entorhinal cortex in PWH compared with controls (A). Within this cluster, a significant negative correlation was present between perceived stress (B,C), post-traumatic stress (D), and depression (E) with metabolic activity. (2) Perceived, chronic, and post-traumatic stress, as well as depression, were negatively correlated with amygdala and hippocampal metabolic activity. (3 Carotid inflammation was positively correlated with perceived and chronic stress but not with glucose metabolism in stress-related brain regions. Aorta inflammation was significantly associated with metabolic activity in dorsolateral and medial prefrontal regions.
IAS: Poor sleep quality in people with HIV linked to lower CSF amyloid beta 42 - (07/26/21)
Sleep aids amyloid beta peptide (Aβ42) clearance from brain, an effect attributed to cerebral glymphatics* Aβ42 accumulates in cerebrospinal fluid (CSF) during wakefulness in multiple clinical populations and declines during normal sleep•Poor sleep quality increases the risk of Alzheimer's Disease (AD)** Those with AD have both poorer sleep quality and lower levels of cerebrospinal fluid (CSF) Aβ42, than healthy elderly, reflecting greater brain tissue amyloid deposition•How sleep is related Aβ42 in people with HIV (PWH) is not known We assessed CSF Aβ42 in relation to sleep quality in PWH, hypothesizing that poorer sleep quality would reduce clearance of amyloid from brain tissue, a phenomenon which, in the context of AD is associated with lower CSF Aβ42 due to a putative selective incorporation of amyloid into plaques, removing it from interstitial spaces and CSF.
Participants: 20 virally suppressed PWH, 15% female, 65% non-Hispanic white, 10% black, mean (SD) age 63.7 (8.1). (Table)
•Median nadir and current CD4 136 and 541.
•Poor sleep quality (PSQI > 5): 11/20 (55%)
•Poorer sleep quality correlated with lower CSF Aβ42 (r = -0.491, p = 0.0278) (Figure 1)
•Sleep quality not related to CSF total Tau or to plasma Aβ42 (Figures 2, 3)
•Age not related to PSQI or CSF Aβ42
•Poorer sleep quality correlated with worse depressed mood (higher BDI-II scores; r = 0.525, p = 0.0174)

•Worsening sleep quality was linked to reduced CSF Aβ42, a pattern similar to that seen in AD
•The association of sleep quality with CSF Aβ42 was specific; PSQI was not related to other CSF biomarkers or to plasma Aβ42
•Lower CSF Aβ42 may reflect greater cerebral amyloid deposition, possibly indicating a greater risk of subsequent AD in PWH
•Interventions that improve sleep in PWH might enhance cerebral amyloid clearance
IAS: Metabolics, Comorbidities & Aging at IAS 2021 - (08/16/21)