This study aimed to assess the global, regional and national burden of pulmonary arterial hypertension (PAH) from 1990 to 2021 using data from the Global Burden of Disease Study 2021. The focus was on evaluating trends in incidence, prevalence, mortality and disability-adjusted life-years (DALYs) associated with PAH and examining these trends by age, gender and sociodemographic index (SDI).

This is a systematic analysis leveraging data from the Global Burden of Disease Study 2021. The analysis focused on both crude and age-standardised rates to track temporal trends in PAH burden, with data stratified by region and SDI.

The study used global, regiona, and national data from 204 countries and regions, spanning from 1990 to 2021.

The participants in this study include individuals diagnosed with PAH, with data representing populations globally, categorised by age, gender and SDI.

Primary outcome measures included global, regional and national incidence, prevalence, mortality and DALYs related to PAH. Secondary outcomes consisted of age-standardised rates (age-standardised incidence rate (ASIR), age-standardised mortality rate (ASMR)) and trends over the study period. A key strength of this study is the detailed stratification by SDI, revealing how PAH burden varies across different socio-economic settings. This extended temporal analysis offers new insights into long-term trends, highlighting the rising burden in lower-SDI regions and significant regional disparities in disease management and outcomes.

From 1990 to 2021, global PAH cases showed substantial increases in both incidence (85.62%) and prevalence (81.46%), while age-standardised rates remained stable. Across SDI levels, high-SDI regions maintained stable ASIRs (0.37 per 100 000) with a slight decline (estimated average percentage change (EAPC) -0.06%), while low-SDI regions demonstrated the most significant reduction (EAPC -0.30%). Deaths increased by 48.36% globally, though the ASMR decreased from 0.35 to 0.27 per 100 000. The disease burden measured by DALYs decreased by 6.59%, with high-SDI regions showing better improvements in age-standardised DALY rates (-1.39% EAPC) compared with other SDI levels. Gender analysis revealed persistent female predominance (female-to-male ratio 1.62:1), particularly pronounced in populations over 50 years across all SDI quintiles.

While global age-standardised rates have declined, PAH remains a significant global health burden, particularly in low-SDI regions. These findings underscore the need for targeted prevention and intervention strategies, especially for high-risk populations, such as females and the elderly, to reduce the global health impact of PAH.

HIV-1 particles are captured by the immunoglobulin superfamily member Siglec-1 on the surface of macrophages and dendritic cells, leading to particle internalization and facilitating trans-infection of CD4+ T cells. HIV-1-infected macrophages develop a unique intracellular compartment termed the virus-containing compartment (VCC) that exhibits characteristic markers of the late endosome and is enriched in components of the plasma membrane (PM). The VCC has been proposed as the major site of particle assembly in macrophages. Depleting Siglec-1 from macrophages significantly reduces VCC formation, implying a link between the capture and uptake of external HIV-1 particles and the development of VCCs within HIV-infected cells. We found that internalization of particles to the VCC was independent of clathrin, but required dynamin-2. CD98 and CD44, classical markers of the CLIC/GEEC pathway, colocalized with Siglec-1 and HIV-1 particles within the VCC. Virus-like particles (VLPs) were taken up within CD98 and Siglec-1-enriched tubular membranes that migrated centripetally over time to form VCC-like structures. Inhibition of CLIC/GEEC-mediated endocytosis resulted in the arrest of captured HIV-1 particles on the macrophage cell surface, prevented VCC formation, and significantly reduced the efficiency of trans-infection of T cells. These findings indicate that following capture of virus by Siglec-1, particles follow an endocytic route to the VCC that requires both the CLIC/GEEC pathway and dynamin-2. We propose a model in which internalization of HIV-1 particles together with CLIC/GEEC membranes leads to the formation of the VCC in HIV-infected macrophages, creating an intracellular platform that facilitates further particle assembly and budding.

Patients with chronic HIV infection face a high risk of premature coronary atherosclerosis, partly due to continuous HAART therapy and susceptibility to opportunistic infections, complicating percutaneous coronary intervention (PCI). HIV patients have unique coronary vasculature characteristics. This study aimed to assess the clinical outcomes of PCI using the novel tapered sirolimus-eluting coronary stent (SES) system in HIV patients.

A prospective, single-arm, non-randomized study was conducted at a tertiary cardiac care center, including 15 HIV-positive patients with acute coronary syndromes. PCI was performed using the study device for de novo coronary lesions with significant size disparity between reference vessel segments. The cumulative incidence of major adverse cardiovascular events (MACE), defined as cardiac death, myocardial infarction, and clinically driven target-lesion revascularization (CD-TLR), was the primary endpoint.

Since 2018, 15 HIV-positive patients with a mean age of 50.67 years underwent PCI with the study device. Despite cardiac risk factors and complex lesions, 100 % procedural and device success was achieved by restoring myocardial flow (TIMI flow III). Over a median follow-up of 40 months, no MACE or adverse events were recorded.

This study provides new evidence on the use of the long, tapered SES for treating HIV-positive patients, demonstrating high success rates and favorable long-term outcomes. It is the first report of such outcomes using a long, tapered SES in this population.

Globally, uncertainty persists regarding the prevalence of comorbidities in noncommunicable diseases (NCDs) among people living with HIV (PLWH) compared those without HIV. This uncertainty extends to the degree of nonrandom associations between comorbidities in both populations, particularly in resource-limited settings.

This cross-sectional study involved 343 HIV-infected individuals (cases) and 686 HIV-uninfected counterparts (controls), with a 1:2 individual matching ratio. Nonrandom associations between comorbidities were assessed using Somers' D statistic.

Comorbidity prevalence was significantly higher in cases (48.7%, 95% confidence interval [CI]: 43.4%-54.0%) than in controls (26.8%, 95% CI: 23.5%-30.1%). Cases exhibited more comorbidities than controls (6 and 4, respectively). Depression, cardiovascular diseases, chronic liver disease, chronic kidney disease, and chronic renal insufficiency were more prevalent among cases (25.7%, 7.9%, 11.1%, 3.5%, 2.0%, respectively) compared to controls. No significant differences were observed in the prevalence of diabetes mellitus, hypertension, chronic obstructive pulmonary disease, and musculoskeletal disorders between the two populations (cases: 7.9%, 12.5%, 0.3%, 6.4%, respectively; controls: 5.1%, 15.6%, 0.1%, 3.9%, respectively). Nonrandom associations between comorbidities were statistically significant in both groups, with Somers' D values ranging from 0.101 to 0.982 in cases and from 0.102 to 0.472 in controls.

The HIV-infected population demonstrates a higher prevalence of comorbidities compared to the HIV-uninfected population. Nonrandom associations between comorbidities exist in both populations, with stronger associations observed among PLWH.

People with HIV (PWH) receiving antiretroviral therapy (ART), despite a similar life expectancy, have a higher incidence of comorbidities than the general population. This study assessed the influence of proinflammatory biomarkers and clinical factors on mortality of PWH. We included PWH hospitalized from 2009 to 2014 who continued ART until 2023. The baseline lipid profile, CD4+ cell count, platelets, CRP, PCT, TNF-α, VCAM-1, and HCV and HBV coinfection were evaluated. Multivariable logistic regression was used to evaluate factors associated with mortality. Among 72 PWH, 19 were lost to a follow-up and 13 died before 2023. The mean follow-up was 12.07 years, while the mean time to death was 4.32 years. The main causes of death were cancer (n = 7) and drug-related death (n = 4). In the multivariate analysis, HCV coinfection, CRP ≥ 5 mg/L, PCT ≥ 0.05 ng/mL, and VCAM-1 ≥ 922 ng/mL were associated with higher odds of death. Although people who died had lower total cholesterol and triglyceride concentrations, these parameters were not associated with mortality. Determining HCV coinfections and CRP, PCT, and VCAM-1 levels may help identify PWH at increased risk of death for intensified monitoring. Care should also be taken of PWH with normal lipid parameters.

Cardiovascular disease (CVD) represents a major cause of premature mortality in people living with HIV (PLWH). There is a need to characterize the cardiovascular health profiles of PLWH to appropriately guide primary prevention efforts, particularly in settings like Sub-Saharan Africa, where there is a high burden of HIV and limited resources. A cross-sectional analysis was conducted on a cohort of newly diagnosed PLWH and HIV-uninfected adults recruited from three HIV clinics in Mwanza, Tanzania. Modified Life's Simple 7 definitions were applied to the cohort to compare cardiovascular health profiles between the two study groups using Poisson regressions. Pooled cohort equation (PCE) scores were also calculated to compare the distribution of CVD risk between the two groups. Our study included 995 study participants (492 PLWH, 503 HIV-uninfected). PLWH had a higher prevalence of ideal body mass index (75%), ideal blood pressure (56%), and ideal total cholesterol but a lower prevalence of ideal smoking (84%) and ideal physical activity (39%) than HIV-uninfected counterparts. PCE scores were low throughout the study population (76.5%), regardless of HIV status. Primary prevention of CVD in newly diagnosed people living with HIV in Africa may need to focus on smoking cessation and optimization of physical activity levels.

People living with HIV are at higher risk of heart failure and associated left atrial remodeling compared to people without HIV. Mechanisms are unclear but have been linked to inflammation and premature aging. Here we obtain plasma proteomics concurrently with cardiac magnetic resonance imaging in two independent study populations to identify parallels between HIV-related and aging-related immune dysfunction that could contribute to atrial remodeling and clinical heart failure. We discover a plasma proteomic signature that may in part reflect or contribute to HIV-associated atrial remodeling, many features of which are associated with older age and time to incident heart failure among an independent community-based cohort without HIV. This proteomic profile was statistically enriched for immune checkpoint proteins, tumor necrosis factor signaling, ephrin signaling, and extracellular matrix organization, identifying possible shared pathways in HIV and aging that may contribute to risk of heart failure.

The increasing lifespan of people living with HIV (PLWH) due to advancements in antiretroviral therapy (ART) has shifted mortality patterns from AIDS-related to non-AIDS-related causes, notably cardiovascular diseases (CVDs). This review investigates how HIV and ART contribute to vascular endothelial dysfunction, myocardial fibrosis, and hypercoagulation, which significantly exacerbate cardiovascular risk. Mechanistic insights include chronic inflammation and immune dysregulation due to persistent HIV infection and ART-specific effects such as protease inhibitors causing dyslipidemia and zidovudine inducing mitochondrial toxicity leading to cardiomyopathy. ART, while lifesaving, has been implicated in promoting subclinical atherosclerosis and increasing the risk of acute myocardial infarction, further highlighting the need for tailored approaches. The manuscript addresses pressing obstacles, including disparities in healthcare access and the lack of standardized cardiovascular screening guidelines specific to PLWH. It emphasizes the integration of advanced imaging techniques and emerging biomarkers, such as coronary artery calcium scoring and soluble ST2, to detect early subclinical cardiovascular abnormalities. The review also identifies challenges in ART selection to balance virologic control and cardiovascular safety. What sets this review apart is its holistic and detailed approach to the intersection of HIV and cardiovascular health. It not only elucidates complex pathophysiological mechanisms but also offers actionable insights into how current clinical guidelines fall short. This manuscript underscores the urgency of implementing proactive cardiovascular screening protocols tailored for PLWH and refining ART regimens to mitigate CVD risks. By addressing these gaps, this work aims to expand our understanding of HIV-related cardiovascular manifestations and provide a foundation for targeted interventions, thereby improving long-term health outcomes for PLWH. This comprehensive perspective is poised to transform clinical practice by fostering greater awareness among physicians and encouraging the development of more effective strategies for managing cardiovascular risks in the HIV population.

Following ischemic stroke, non-neuronal cells within the nervous system play a crucial role in maintaining neurovascular unit functions, regulating metabolic and inflammatory processes of the nervous system. Investigating the functions and regulation of these cells, particularly immune cells, deepens our understanding of the complex mechanisms of neuroinflammation and immune modulation after ischemic stroke and provides new perspectives and methods for immune-related therapy.

The annual distribution, journals, authors, countries, institutions, and keywords of articles published between 2015 and 2024 were visualized and analyzed using CiteSpace and other bibliometric tools.

A total of 1,089 relevant articles or reviews were included, demonstrating an overall upward trend; The terms "cerebral ischemia," "immune response," "brain ischemia," "cerebral inflammation," "neurovascular unit," and "immune infiltration," etc. are hot keywords in this field.

In recent years, research on immune-related therapy for ischemic stroke has focused on mechanisms of occurrence, protection and repair of the blood-brain barrier (BBB) by non-neuronal cells, and regulation of immunosuppression and inflammation. Among these, reducing BBB disruption to minimize secondary brain damage has become a hotspot. At the same time, the complex roles of immune responses have attracted attention, particularly the balance between regulatory T cells and Th17 cells in regulating neuroinflammation and promoting neurological function recovery, which is crucial to reduce secondary neuronal damage and improve prognosis, potentially establishing a pivotal frontier in this domain of investigation.

Body weight is impacted by several individual host and environmental factors. In a person living with HIV (PLWH), weight is also influenced by the disease stage. Wasting syndrome is derived from disease progression, and it can be reversed by the effective use of highly active antiretroviral therapy (HAART). Body weight alterations have been studied and compared in several clinical ART trials, and they differ according to antiviral regimens. The newer integrase strand transfer inhibitors (INSTIs), such as bictegravir and dolutegravir, especially when co-administered with tenofovir alafenamide fumarate (TAF), seem to lead to greater weight increases compared to regimens that include tenofovir disoproxil fumarate (TDF), which seem to have an attenuating effect on weight gain. Nevertheless, despite the established association between INSTI and TAF and the negative impact on weight, more recent data suggest a more cautious approach when HAART treatment decisions are taken. In this manuscript, we review weight changes among PLWH receiving HAART and the relevant underlying pathogenic mechanisms described in recent literature. We try to provide a more critical appraisal of the available data and to underline the challenges in assessing the role of HAART in weight changes in both ART initiation and setting switching.

HIV-associated cardiovascular diseases remain a leading cause of death in people living with HIV/AIDS (PLWHA). Although antiretroviral drugs suppress the viral load, they fail to remove the virus entirely. HIV-1 Nef protein is known to play a role in viral virulence and HIV latency. Expression of Nef protein can be detected in different organs, including cardiac tissue. Despite the established role of Nef protein in HIV-1 replication, its impact on organ function inside the human body is not clear. To understand the effect of Nef at the organ level, we created a new Nef-transgenic (Nef-TG) mouse that expresses Nef protein in the heart. Our study found that Nef expression caused inhibition of cardiac function and pathological changes in the heart with increased fibrosis, leading to heart failure and early mortality. Further, we found that cellular autophagy is significantly inhibited in the cardiac tissue of Nef-TG mice. Mechanistically, we found that Nef protein causes the accumulation of Bcl2 and Beclin-1 proteins in the tissue, which may affect the cellular autophagy system. Additionally, we found Nef expression causes upregulation of the cellular senescence marker p21 and senescence-associated β-galactosidase expression. Our findings suggest that the Nef-mediated inhibition of autophagy and induction of senescence markers may promote aging in PLWHA. Our mouse model could help us to understand the effect of Nef protein on organ function during latent HIV infection.

We aimed to demonstrate the use of quantitative bias analysis (QBA), which reveals the effects of systematic error, including confounding, misclassification and selection bias, on study results in epidemiological studies published in the period from 2010 to mid-23.

The articles identified through a keyword search using Pubmed and Scopus were included in the study. The articles obtained from this search were eliminated according to the exclusion criteria, and the articles in which QBA analysis was applied were included in the detailed evaluation.

It can be said that the application of QBA analysis has gradually increased over the 13-year period. Accordingly, the number of articles in which simple is used as a method in QBA analysis is 9 (9.89%), the number of articles in which the multidimensional approach is used is 10 (10.99%), the number of articles in which the probabilistic approach is used is 60 (65.93%) and the number of articles in which the method is not specified is 12 (13.19%). The number of articles with misclassification bias model is 44 (48.35%), the number of articles with uncontrolled confounder(s) bias model is 32 (35.16%), the number of articles with selection bias model is 7 (7.69%) and the number of articles using more than one bias model is 8 (8.79%). Of the 49 (53.85%) articles in which the bias parameter source was specified, 19 (38.78%) used internal validation, 26 (53.06%) used external validation and 4 (8.16%) used educated guess, data constraints and hypothetical data. Probabilistic approach was used as a bias method in 60 (65.93%) of the articles, and mostly beta (8 [13.33%)], normal (9 [15.00%]) and uniform (8 [13.33%]) distributions were selected.

The application of QBA is rare in the literature but is increasing over time. Future researchers should include detailed analyzes such as QBA analysis to obtain inferences with higher evidence value, taking into account systematic errors.

Cardiovascular disease is a major cause of morbidity in an aging HIV population. However, risk estimation with the most frequent equations usually classifies HIV patients as having a low or moderate risk. Several studies have described a very high prevalence of subclinical atherosclerosis in a middle-aged, non-HIV population. There is insufficient body of knowledge to understand if this is the case in people living with HIV (PLWH). We aim to calculate the proportion of patients with subclinical atherosclerosis in a single site cohort of HIV-infected subjects.

We have analyzed chronically HIV infected adults (≥ 18 years) who were on active follow-up in an HIV unit specialized in the care of cardiovascular health. The most recent clinical visit and vascular ultrasonography were used to assess the objectives of our research. Our primary objective was to describe the proportion of participants with subclinical atherosclerosis (focal protrusion into the lumen > 0.5 mm or > 50% of the surrounding IMT or a diffuse thickness > 1.5 mm) in a single site cohort of PLWH. Carotid and iliofemoral territories were evaluated. As a secondary objective we have run a multivariate analysis to determine which HIV and non-HIV factors might be related with the presence of atherosclerotic plaques. Findings We included a total of 463 participants between November 2017 to October 2019. Subjects were predominantly male (84.2%) with a mean age of 48.8 years (SD 10.7). Hypercholesterolemia (36%) was the most prevalent comorbidity followed by Hypertension (18%) and Hypertriglyceridemia (16%). Mean duration of HIV infection is 12.3 years. Overall, participants had been receiving cART for a median of 9.5 years. Subclinical atherosclerosis was found in 197 subjects (42.5%; CI 95% [38.0-47.2]). The disease was found more frequently in the femoral arteries (37.8%) than in the carotid vascular bed (18.6%). Despite some HIV factors correlated with the presence of plaques in a univariate analysis (e.g., time with HIV-1 RNA > 50 copies/mL or time from HIV diagnosis), the only two explanatory factors that remained associated with the presence of atherosclerotic plaques in the multivariate analysis were smoking (OR 5.47, 95% CI 3.36 - 8.90) and age (OR 1.13, 95%CI 1.10 - 1.16). Interpretation We have found a very high prevalence of subclinical atherosclerosis among our cohort of PLWH. Despite having analyzed several HIV factors, age and smoking have been found to be the only factors associated with the development of atherosclerotic plaques.

Hepatic steatosis is highly prevalent in people living with HIV. It remains unclear whether HIV in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with greater risks of liver disease progression and cardiovascular disease (CVD). We aim to evaluate the impact of HIV infection on risks of liver and CVD outcomes among US Veterans with MASLD.

Using national Veterans Administration data from 2010 to 2022, we created a propensity score-matched cohort of MASLD patients with vs without HIV. Primary outcomes were incidence of cirrhosis and hepatocellular carcinoma (HCC) among patients with vs without HIV and patients with MASLD-HIV on antiretroviral therapy (ART) vs not on ART. Secondary outcomes included incidence of major adverse cardiovascular events and overall survival.

The propensity-matched cohort included 920 MASLD patients with HIV and 920 MASLD patients without HIV and was similar in demographics and comorbidities. Compared with MASLD patients without HIV, incidences of cirrhosis and HCC were similar among MASLD with HIV. Compared with MASLD patients without HIV, incidence of major adverse cardiovascular event was higher among MASLD patients with HIV (5.18 vs 4.48 per 100 person-years, P = 0.03). Overall 5-year survival was significantly lower among MASLD patients with HIV and even lower among those not on ART.

Among US Veterans with MASLD, concurrent HIV infection, and particularly not being on ART, is associated with greater risks of CVD and decreased overall survival. No differences in risks of cirrhosis or HCC were observed.

HIV infection is a multi-organ disease that involves the central nervous system (CNS). While devastating CNS complications such as HIV-associated dementia and CNS opportunistic infection typically manifest years after HIV acquisition, HIV RNA is readily detected in the cerebrospinal fluid in untreated neuroasymptomatic people with HIV, highlighting that HIV neuroinvasion predates overt clinical manifestations. Over the past two decades, increased awareness of HIV infection within the at-risk population, coupled with the accessibility of nucleic acid testing and modern HIV immunoassays, has made the detection of acute and early HIV infection readily achievable. This review aims to summarize research findings on CNS involvement during acute and early HIV infection, as well as the outcomes following the immediate initiation of antiretroviral therapy during this early stage of infection. The knowledge gap in long-term neuroprotection through early ART within the first year of infection will be discussed.

Despite modern antiretroviral therapy (ART), people living with HIV (PLWH) have increased relative risk of inflammatory-driven comorbidities, including cardiovascular disease (CVD). The gut microbiome could be one of several driving factors, along with traditional risk factors and HIV-related risk factors such as coinfections, ART toxicity, and past immunodeficiency.

PLWH have an altered gut microbiome, even after adjustment for known confounding factors including sexual preference. The HIV-related microbiome has been associated with cardiometabolic comorbidities, and shares features with CVD-related microbiota profiles, in particular reduced capacity for short-chain fatty acid (SCFA) generation. Substantial inter-individual variation has so far been an obstacle for applying microbiota profiles for risk stratification. This review covers updated knowledge and recent advances in our understanding of the gut microbiome and comorbidities in PLWH, with specific focus on cardiometabolic comorbidities and inflammation. It covers a comprehensive overview of HIV-related and comorbidity-related dysbiosis, microbial translocation, and microbiota-derived metabolites. It also contains recent data from studies in PLWH on circulating metabolites related to comorbidities and underlying gut microbiota alterations, including circulating levels of the SCFA propionate, the histidine-analogue imidazole propionate, and the protective metabolite indole-3-propionic acid.

Despite recent advances, the gut microbiome and related metabolites are not yet established as biomarkers or therapeutic targets. The review gives directions for future research needed to advance the field into clinical practice, including promises and pitfalls for precision medicine. Video Abstract.

HIV type 1 (HIV-1) is the causative agent of AIDS. Since the start of the epidemic, HIV/AIDS has been responsible for ≈40 million deaths. Additionally, an estimated 39 million people are currently infected with the virus. HIV-1 primarily infects immune cells, such as CD4+ (cluster of differentiation 4+) T lymphocytes (T cells), and as a consequence, the number of CD4+ T cells progressively declines in people living with HIV. Within a span of ≈10 years, HIV-1 infection leads to the systemic failure of the immune system and progression to AIDS. Fortunately, potent antiviral therapy effectively controls HIV-1 infection and prevents AIDS-related deaths. The efficacy of the current antiviral therapy regimens has transformed the outcome of HIV/AIDS from a death sentence to a chronic disease with a prolonged lifespan of people living with HIV. However, antiviral therapy is not curative, is challenged by virus resistance, can be toxic, and, most importantly, requires lifelong adherence. Furthermore, the improved lifespan has resulted in an increased incidence of non-AIDS-related morbidities in people living with HIV including cardiovascular diseases, renal disease, liver disease, bone disease, cancer, and neurological conditions. In this review, we summarize the current state of knowledge of the cardiovascular comorbidities associated with HIV-1 infection, with a particular focus on hypertension. We also discuss the potential mechanisms known to drive HIV-1-associated hypertension and the knowledge gaps in our understanding of this comorbid condition. Finally, we suggest several directions of future research to better understand the factors, pathways, and mechanisms underlying HIV-1-associated hypertension in the post-antiviral therapy era.

HIV infection and antiretroviral therapy alter mitochondrial function, which can progressively lead to mitochondrial damage and accelerated aging. The interaction between persistent HIV reservoirs and mitochondria may provide insight into the relatively high rates of cardiovascular disease and mortality in persons living with HIV. In this review, we explore the intricate relationship between HIV and mitochondrial function, highlighting the potential for novel therapeutic strategies in the context of cardiovascular diseases. We reflect on mitochondrial dynamics, mitochondrial DNA, and mitochondrial antiviral signaling protein in the context of HIV. Furthermore, we summarize how toxicities related to early antiretroviral therapy and current highly active antiretroviral therapy can contribute to mitochondrial dysregulation, chronic inflammation, and poor clinical outcomes. There is a need to understand the mechanisms and develop new targeted therapies. We further consider current and potential future therapies for HIV and their interplay with mitochondria. We reflect on the next-generation antiretroviral therapies and HIV cure due to the direct and indirect effects of HIV persistence, associated comorbidities, coinfections, and the advancement of interdisciplinary research fields. This includes exploring novel and creative approaches to target mitochondria for therapeutic intervention.

Although AIDS-related deaths have reduced with increased access to antiretroviral care, cardiovascular disease-related morbidities among persons living with HIV are rising. Contributing to this is the higher incidence of Hypertension among Persons Living with HIV. The duration of exposure to the virus and antiretroviral drugs plays a vital role in the pathogenesis, putting perinatally infected children and adolescents at higher risk than behaviorally-infected ones, supporting the calls for increased surveillance of Hypertension among them. Despite the availability of guidelines to support this surveillance, the blood pressure (BP) of adolescents living with HIV (ADLHIV) is not checked during clinical visits. This study aims to assess the effect of a theory-based intervention on healthcare workers' adherence to the guidelines for hypertension screening among adolescents.

A multi-facility cluster-randomized study will be conducted. The clusters will be 20 antiretroviral therapy sites in the Greater Accra Region of Ghana with the highest adolescent caseload. Data will be extracted from the folders of adolescents (10-17 years) who received care in these facilities six months before the study. The ART staff of intervention facilities will receive a multicomponent theory of planned behaviour-based intervention. This will include orientation on hypertension risk among ADLHIV, provision of job aids and pediatric sphygmomanometers. Six months after the intervention, the outcome measure will be the change from baseline in the proportion of ADLHIV whose BP was checked during clinical visits. The calculated sample size is 400 folders.

This study will generate evidence on the effectiveness of a multicomponent theory-based intervention for improving the implementation of clinical practice guidelines.

PACTR202205641023383.

Physical activity could increase the production of oxidative stress biomarkers, affecting the metabolism and excretion of antiretroviral drugs and, consequently, the clinical outcome. Nowadays, people living with HIV (PLWH) are mostly switching from triple to dual therapy, but no data are available in terms of physical functioning and oxidative stress. The aim of this study was to evaluate if some antioxidant biomarkers and physical functioning tests could be different according to triple or dual antiretroviral therapy.

PLWH were evaluated at baseline (BL), while treated with three drugs, and six months after the switch to dual therapy. Physical functioning was quantified using validated tools. Mitochondrial and cytosol antioxidant molecules were evaluated through liquid chromatography.

Twenty-five patients were analyzed. A statistically significant difference between triple and dual therapy was found for mitochondrial glutathione, but not for physical tests. Evaluating differences between physically active and inactive individuals, the following statistically significant differences were suggested, considering triple therapy (mitochondrial n-formyl-methionine p = 0.022, triglycerides p = 0.023) and double therapy (mitochondrial glycine p = 0.035, cytosol glutamic acid p = 0.007, cytosol s-adenosylmethionine p = 0.021).

For the first time, this study suggests possible differences in terms of antioxidant molecules and physical functioning in PLWH switching from triple to dual therapy.

The prognosis of AIDS after active antiretroviral therapy (ART) and the quality of life of people living with HIV (PLWH) are both affected by non-AIDS-related diseases such as cardiovascular disease (CVD). However, the specific risk ratios between PLWH and individuals negative for HIV are poorly understood. We aimed to systematically review and investigate the CVD risk factors associated with HIV.

We searched PubMed, Embase, Web of Science, and Cochrane Library databases between 1 January 2015, and 12 May 2023 for articles reported the prevalence and risk factors of CVD such as hypertension, dyslipidaemia, coronary artery disease (CAD), and myocardial infarction (MI). Due to the high heterogeneity, we used a random-effects model to analyse the data. All statistical analyses were performed using Stata/MP 17.0 with 95% confidence intervals (CIs).

We analysed 31 eligible studies including 312 913 PLWH. People living with HIV had higher risks of dyslipidaemia (hazard ratio (HR) = 1.53; 95% CI = 1.29, 1.82), CAD (HR = 1.37; 95% CI = 1.24, 1.51), and MI (HR = 1.47; 95% CI = 1.28, 1.68) compared to individuals without HIV. However, there were no significant differences in the prevalence of hypertension between groups (HR = 1.17; 95% CI = 0.97, 1.41). Subgroup analysis revealed that men with HIV, PLWH who smoked and the elderly PLWH had a high prevalence of CVD. Moreover, the disease prevalence patterns varied among regions. In the USA and Europe, for instance, some HRs for CVD were higher than in other regions. Active ART initiation after 2015 appears to have a lower risk of CVD (hypertension, hyperlipidaemia, CAD). All outcomes under analysis showed significant heterogeneity (I2>70%, P < 0.001), which the available study-level variables could only partially account for.

People living with HIV had a higher CVD risk than the general population; thus, CVD prevention in PLWH requires further attention. Rapid initiation of ART may reduce the incidence of CVD in PLWH. For timely screening of CVD high-risk individuals and thorough disease management to prevent CVD, further studies are required to evaluate the risk factors for CVD among PLWH, such as age, region, etc.

PROSPERO (CRD42021255508).

This study aims to investigate the incidence and dynamic risk factors for cardiovascular diseases (CVD) among people living with HIV (PLWH).

In this population-based statewide cohort study, we utilized integrated electronic health records data to identify adult (age ≥ 18) who were diagnosed with HIV between 2006 and 2019 and were CVD event-free at the HIV diagnosis in South Carolina. The associations of HIV-related factors and traditional risk factors with the CVD incidence were investigated during the overall study period, and by different follow-up periods (i.e., 0-5yrs, 6-10yrs 11-15yrs) using multivariable logistic regression models.

Among 9,082 eligible participants, the incidence of CVD was 18.64 cases per 1000 person-years. Overall, conventional risk factors, such as tobacco use, hypertension, obesity, chronic kidney disease (CKD), were persistently associated with the outcome across all three groups. While HIV-related factors, such as recent CD4 count (e.g., > 350 vs. <200 cells/mm3: adjusted odds ratio [aOR] range: 0.18-0.25), and percent of years in retention (e.g., 31-75% vs. 0-30%: aOR range: 0.24-0.57) were associated with lower odds of CVD incidence regardless of different follow up periods. The impact of the percent of days with viral suppression gradually diminished as the follow-up period increased.

Maintaining an optimal viral suppression might prevent CVD incidence in the short term, whereas restoring immune recovery may be beneficial for reducing CVD risk regardless of the duration of HIV diagnosis. Our findings suggest the necessity of conducting more targeted interventions during different periods of HIV infection.

This randomized controlled trial study aimed to investigate the effectiveness of therapeutic lifestyle change (TLC) diet intervention by the registered dietitians.

Eighty-two people living with HIV (PLHIV) with dyslipidemia were randomly allocated to the intervention group as well as another 82 PLHIV with dyslipidemia to the control group. Participants in the intervention group were instructed to meet the registered dietitians every 2 weeks at weeks 0, 2, 4, 6, and 12 (a totally of 12 weeks) to receive individual medical nutrition therapy according to the TLC diet principles, while the participants in the control group only received routine health care service.

Triglycerides, total cholesterol, and LDL cholesterol of the intervention group were significantly lower than those of the control group at the endpoint (p < 0.05). In addition, these biomarkers and C-reactive protein of the intervention group were significantly lower when compared with their baseline (p < 0.05). The overall dietary habits of participants in the intervention group were significantly improved at the end of the study (p < 0.05).

The medical nutrition therapy intervention based on the TLC diet is effective in improving blood lipid profiles among PLHIV with dyslipidemia.

People living with HIV (PLWH) may be at heightened risk for cardiovascular disease (CVD). Statin use and lifestyle changes reduce the risk of CVD but remain under-prescribed among PLWH. The objective of this study was to characterize knowledge of CVD and statin use, current usage, barriers to taking statins, and information desired by PLWH to improve statin uptake among PLWH in Los Angeles, CA.

Between April 2019 and April 2020, we conducted four focus group discussions (n = 37) with patients across three public community health clinics that serve PLWH in Los Angeles County, California. All clinics participated in a larger study to improve statin prescribing for PLWH. We asked about knowledge of statins, willingness to take a statin, possible barriers to statin usage, preferred information sources for health information, and desired information about statins. We utilized standard qualitative content analysis methods to identify themes.

We found a range in the awareness of statins, with some participants reporting never having heard of statins while others had a history of statin use. There were concerns about the potential long-term effect of statin use, but participants expressed willingness to use CVD medications generally and statins specifically, especially if recommended by their healthcare provider. Participants also expressed interest in potential alternatives to statin usage such as exercising regularly and nutritious eating.

More interventions are needed to increase statin use among PLWH to improve CVD outcomes, which also has implications for HIV progression. Clinics should aim to increase patient and provider knowledge about CVD risk and statin use for PLWH and provide shared decision-making tools that are easy to use and culturally appropriate.

Vascular aging, a precursor of arterial stiffness, is associated with neurocognitive impairment (NCI) and cardiovascular disease. Although HIV is associated with rapid vascular aging, it is unknown whether arterial stiffness mediates changes in cognitive function. We explored whether estimated markers of vascular aging were associated with NCI indices in HIV-positive individuals.

This study was a secondary analysis of an observational study. Neurocognitive functioning was assessed using a battery of 7 domains (verbal fluency, executive functioning, speed of information processing, attention/working memory, memory [learning and delayed recall], and motor skills). Vascular aging was assessed using estimated markers of arterial stiffness (ie, estimated pulse wave velocity, pulse pressure, and vascular overload index). A multivariable regression adjusted for demographics, cardiovascular disease risk factors, and HIV clinical variables was used to examine the association between vascular aging and NCI outcomes.

Among 165 people with HIV, the mean age was 51.5 ± 6.9 years (62% men and 83% African American/Black or Other). In fully adjusted models, an increase in estimated pulse wave velocity and pulse pressure was associated with lower T scores in learning (-2.95 [-5.13, -0.77]) and working memory (-2.37 [-4.36, -0.37]), respectively. An increase in vascular overload index was associated with lower T scores in working memory (-2.33 [-4.37, -0.29]) and learning (-1.85 [-3.49, -0.21]).

Estimated markers of arterial stiffness were weakly associated with neurocognitive functioning, suggesting that vascular aging may have a role in cognitive decline among people with HIV.

Antiretroviral therapies (ART) have reduced human immunodeficiency virus (HIV) infection-associated morbidity and mortality improving the life of people with HIV (PWH). However, ART lead to residual HIV production, which in conjunction with microbial translocation and immune dysfunction contributes to chronic inflammation and immune activation. PWH on ART remain at an increased risk for cardiovascular diseases (CVDs) including myocardial infarction and stroke; which in part is explained by chronic inflammation and immune activation. Lifestyle factors and certain ART are associated with dyslipidemia characterized by an increase of low-density lipoprotein (LDL), which further contributes in the increased risk for CVDs. Lipid-lowering agents like statins are emerging as immune modulators in decreasing inflammation in a variety of conditions including HIV. The international randomized clinical trial REPRIEVE has shed light on the reduction of CVDs with statin therapy among PWH. Such reports indicate a more than expected benefit of statins beyond their lipid-lowering effects. Bempedoic acid, a first-in-class non-statin LDL-lowering drug with immune modulatory effects, may further aid PWH in combination with statins. Herein, we critically reviewed studies aimed at lipid-lowering and immune-modulating roles of statins that may benefit aging PWH.

Medical professionals, particularly in regions with a high burden of human immunodeficiency virus (HIV), should be alert to the hematological complications of HIV, which may include cytopenias, malignancy, and coagulation disturbances. Patients may present with these conditions as the first manifestation of HIV infection. Hematological abnormalities are often multifactorial with opportunistic infections, drugs, malignancy, and HIV infection itself contributing to the clinical presentation, and the diagnosis should consider all these factors. Life-threatening hematological complications requiring urgent diagnosis and management include thrombotic thrombocytopenic purpura, superior mediastinal syndrome, spinal cord compression, and tumor lysis syndrome due to aggressive lymphoma. Antiretroviral therapy is the therapeutic backbone, including for patients with advanced HIV, in addition to specific therapy for the complication. This article reviews the impact of HIV on the hematological system and provides a clinical and diagnostic approach, including the role of a bone marrow biopsy, focusing on perspectives from sub-Saharan Africa.

Human immunodeficiency virus infection (HIV+) is associated with a 2-fold increased risk of cardiovascular disease. Increasingly, patients who are HIV + are being evaluated to undergo cardiac surgery. Current risk-adjusted scoring systems, including the Society of Thoracic Surgeons Predicted Risk of Mortality score, fail to stratify HIV + risk. Unfortunately, there exists a paucity of cardiac surgery outcomes data in modern patients who are HIV+.

We conducted a retrospective review of PearlDiver, an all-payer claims administrative database. In total, 14,714,743 patients were captured between 2010 and 2020. Of these, 59,695 (0.4%) of patients had a history of HIV+, and 1759 (2.95%) of these patients underwent cardiac surgery. Patients who were HIV+ were younger, more often male, and had greater comorbidity, history of hypertension, chronic obstructive pulmonary disease, chronic liver disease, chronic kidney disease, chronic lung disease, and heart failure.

Postoperatively, patients who were HIV + had significantly greater rates of pneumonia (relative risk, 1.70; P = .0003) and 30-day all-cause readmission (relative risk, 1.28, P < .0001). After linear regression analysis, these results remained significant. Data also show that a lesser proportion of patients with HIV + underwent coronary artery bypass grafting, aortic valve replacement, and any cardiac surgery compared with controls.

Patients who are HIV + undergoing cardiac surgery are at greater risk of pneumonia and readmission. Moreover, we discovered lower rates of cardiac surgery in patients who are HIV+, which may reflect limited access to surgery when indicated. Today's risk-adjusted scoring systems in cardiac surgery need to better account for the modern patient who is HIV+.

Heart failure risk is elevated in people with HIV (PWH). We investigated whether initial antiretroviral therapy (ART) regimens influenced heart failure risk.

Cohort study.

PWH who initiated an ART regimen between 2000 and 2016 were identified from three integrated healthcare systems. We evaluated heart failure risk by protease inhibitor, nonnucleoside reverse transcriptase inhibitors (NNRTI), and integrase strand transfer inhibitor (INSTI)-based ART, and comparing two common nucleotide reverse transcriptase inhibitors: tenofovir disoproxil fumarate (tenofovir) and abacavir. Follow-up for each pairwise comparison varied (i.e. 7 years for protease inhibitor vs. NNRTI; 5 years for tenofovir vs. abacavir; 2 years for INSTIs vs. PIs or NNRTIs). Hazard ratios were from working logistic marginal structural models, fitted with inverse probability weighting to adjust for demographics, and traditional cardiovascular risk factors.

Thirteen thousand six hundred and thirty-four PWH were included (88% men, median 40 years of age; 34% non-Hispanic white, 24% non-Hispanic black, and 24% Hispanic). The hazard ratio (95% CI) were: 2.5 (1.5-4.3) for protease inhibitor vs. NNRTI-based ART (reference); 0.5 (0.2-1.8) for protease inhibitor vs. INSTI-based ART (reference); 0.1 (0.1-0.8) for NNRTI vs. INSTI-based ART (reference); and 1.7 (0.5-5.7) for tenofovir vs. abacavir (reference). In more complex models of cumulative incidence that accounted for possible nonproportional hazards over time, the only remaining finding was evidence of a higher risk of heart failure for protease inhibitor compared with NNRTI-based regimens (1.8 vs. 0.8%; P  = 0.002).

PWH initiating protease inhibitors may be at higher risk of heart failure compared with those initiating NNRTIs. Future studies with longer follow-up with INSTI-based and other specific ART are warranted.

Cardiovascular disease, particularly coronary heart disease, is becoming more common among those living with HIV. Individuals with HIV face an increased susceptibility to myocardial infarction, also known as a heart attack, as compared to the general population in developed countries. This heightened risk can be attributed mainly to the presence of effective antiretroviral drugs and the resulting longer lifespan. Some cardiac issues linked to non-antiretroviral medications, including myocarditis, endocarditis, cardiomyopathy with dilation, pulmonary hypertension, and oedema of the heart, may affect those not undergoing highly active antiretroviral therapy (ART). Impaired immune function and systemic inflammation are significant contributors to this phenomenon after initiating highly aggressive antiretroviral treatment ART. It is becoming more challenging to determine the best course of treatment for HIV-associated cardiomyopathy due to new research suggesting that protease inhibitors might have a negative impact on the development of HF. Currently, the primary focus of research on ART medications is centered on the cardiovascular adverse effects of nucleoside reverse transcriptase inhibitors and protease inhibitors. This review paper thoroughly evaluates the advancements achieved in cardiovascular disease research and explores the potential implications for prospects. Additionally, it considers the field's future prospects while examining how ART might be altered and its clinical applications.

People living with HIV (PLWH) are at higher risk of heart failure (HF) and preceding subclinical cardiac abnormalities, including left atrial dilation, compared to people without HIV (PWOH). Hypothesized mechanisms include premature aging linked to chronic immune activation. We leveraged plasma proteomics to identify potential novel contributors to HIV-associated differences in indexed left atrial volume (LAVi) among PLWH and PWOH and externally validated identified proteomic signatures with incident HF among a cohort of older PWOH.

We performed proteomics (Olink Explore 3072) on plasma obtained concurrently with cardiac magnetic resonance imaging among PLWH and PWOH in the United States. Proteins were analyzed individually and as agnostically defined clusters. Cross-sectional associations with HIV and LAVi were estimated using multivariable regression with robust variance. Among an independent general population cohort, we estimated associations between identified signatures and LAVi using linear regression and incident HF using Cox regression.

Among 352 participants (age 55±6 years; 25% female), 61% were PLWH (88% on ART; 73% with undetectable HIV RNA) and mean LAVi was 29±9 mL/m 2 . Of 2594 analyzed proteins, 439 were associated with HIV serostatus, independent of demographics, hepatitis C virus infection, renal function, and substance use (FDR<0.05). We identified 73 of these proteins as candidate contributors to the independent association between positive HIV serostatus and higher LAVi, enriched in tumor necrosis factor (TNF) signaling and immune checkpoint proteins regulating T cell, B cell, and NK cell activation. We identified one protein cluster associated with LAVi and HIV regardless of HIV viral suppression status, which comprised 42 proteins enriched in TNF signaling, ephrin signaling, and extracellular matrix (ECM) organization. This protein cluster and 30 of 73 individual proteins were associated with incident HF among 2273 older PWOH (age 68±9 years; 52% female; 8.5±1.4 years of follow-up).

Proteomic signatures that may contribute to HIV-associated LA remodeling were enriched in immune checkpoint proteins, cytokine signaling, and ECM organization. These signatures were also associated with incident HF among older PWOH, suggesting specific markers of chronic immune activation, systemic inflammation, and fibrosis may identify shared pathways in HIV and aging that contribute to risk of HF.

Mixed glia are infiltrated with HIV-1 virus early in the course of infection leading to the development of a persistent viral reservoir in the central nervous system. Modification of the HIV-1 genome using gene editing techniques, including CRISPR/Cas9, has shown great promise towards eliminating HIV-1 viral reservoirs; whether these techniques are capable of removing HIV-1 viral proteins from mixed glia, however, has not been systematically evaluated. Herein, the efficacy of adeno-associated virus 9 (AAV9)-CRISPR/Cas9 gene editing for eliminating HIV-1 messenger RNA (mRNA) from cortical mixed glia was evaluated in vitro and in vivo. In vitro, a within-subjects experimental design was utilized to treat mixed glia isolated from neonatal HIV-1 transgenic (Tg) rats with varying doses (0, 0.9, 1.8, 2.7, 3.6, 4.5, or 5.4 µL corresponding to a physical titer of 0, 4.23 × 109, 8.46 × 109, 1.269 × 1010, 1.692 × 1010, 2.115 × 1010, and 2.538 × 1010 gc/µL) of CRISPR/Cas9 for 72 h. Dose-dependent decreases in the number of HIV-1 mRNA, quantified using an innovative in situ hybridization technique, were observed in a subset (i.e., n = 5 out of 8) of primary mixed glia. In vivo, HIV-1 Tg rats were retro-orbitally inoculated with CRISPR/Cas9 for two weeks, whereby treatment resulted in profound excision (i.e., approximately 53.2%) of HIV-1 mRNA from the medial prefrontal cortex. Given incomplete excision of the HIV-1 viral genome, the clinical relevance of HIV-1 mRNA knockdown for eliminating neurocognitive impairments was evaluated via examination of temporal processing, a putative neurobehavioral mechanism underlying HIV-1-associated neurocognitive disorders (HAND). Indeed, treatment with CRISPR/Cas9 protractedly, albeit not permanently, restored the developmental trajectory of temporal processing. Proof-of-concept studies, therefore, support the susceptibility of mixed glia to gene editing and the potential of CRISPR/Cas9 to serve as a novel therapeutic strategy for HAND, even in the absence of full viral eradication.

Blood-brain barrier (BBB) breakdown is one of the pathophysiological characteristics of ischemic stroke, which may contribute to the progression of brain tissue damage and subsequent neurological impairment. Human immunodeficiency virus (HIV)-infected individuals are at greater risk for ischemic stroke due to diminished immune function and HIV-associated vasculopathy. Studies have shown that astrocytes are involved in maintaining BBB integrity and facilitating HIV-1 infection in the brain. The present study investigated whether targeting astrocyte-endothelial cell signaling with cenicriviroc (CVC), a dual chemokine receptor (CCR)2 and CCR5 antagonist, may protect against dysregulation of cross talk between these cells after oxygen-glucose deprivation/reoxygenation (OGD/R) combined with HIV-1 infection. Permeability assay with 10 kDa fluorescein isothiocyanate (FITC)-dextran demonstrated that CVC alleviated endothelial barrier disruption in noncontact coculture of human brain microvascular endothelial cells (HBMECs) with HIV-1-infected human astrocytes, and reversed downregulation of tight junction protein claudin-5 induced by OGD/R- and HIV-1. Moreover, CVC attenuated OGD/R- and HIV-1-triggered upregulation of the NOD-like receptor protein-3 (NLRP3) inflammasome and IL-1β secretion. Treatment with CVC also suppressed astrocyte pyroptosis by attenuating cleaved caspase-1 levels and the formation of cleaved N-terminal GSDMD (N-GSDMD). Secretome profiling revealed that CVC ameliorated secretion levels of chemokine CC chemokine ligand 17 (CCL17), adhesion molecule intercellular adhesion molecule-1 (ICAM-1), and T cell activation modulator T cell immunoglobulin and mucin domain 3 (TIM-3) by astrocytes synergistically induced by OGD/R and HIV-1. Overall, these results suggest that CVC contributes to restoring astrocyte-endothelial cross interactions in an astrocyte-dependent manner via protection against NLRP3 activation and pyroptosis.NEW & NOTEWORTHY The present study reveals the role of astrocytic NOD-like receptor protein-3 (NLRP3) inflammasome in dysfunctional astrocyte-endothelial cross interactions triggered in response to oxygen/glucose deprivation injury associated with human immunodeficiency virus type 1 (HIV-1) infection. Our results suggest that blocking NLRP3 inflammasome activation and pyroptosis-mediated inflammation with cenicriviroc (CVC) may constitute a potentially effective therapeutic strategy for blood-brain barrier (BBB) protection during HIV-1-associated ischemic stroke.

The developments in HIV treatments have increased the life expectancy of people living with HIV (PLWH), a situation that makes cardiovascular disease (CVD) in that population as relevant as ever. PLWH are at increased risk of CVD, and our understanding of the underlying mechanisms is continually increasing. HIV infection is associated with elevated levels of multiple proinflammatory molecules, including IL-6, IL-1β, VCAM-1, ICAM-1, TNF-α, TGF-β, osteopontin, sCD14, hs-CRP, and D-dimer. Other currently examined mechanisms include CD4 + lymphocyte depletion, increased intestinal permeability, microbial translocation, and altered cholesterol metabolism. Antiretroviral therapy (ART) leads to decreases in the concentrations of the majority of proinflammatory molecules, although most remain higher than in the general population. Moreover, adverse effects of ART also play an important role in increased CVD risk, especially in the era of rapid advancement of new therapeutical options. Nevertheless, it is currently believed that HIV plays a more significant role in the development of metabolic syndromes than treatment-associated factors. PLWH being more prone to develop CVD is also due to the higher prevalence of smoking and chronic coinfections with viruses such as HCV and HBV. For these reasons, it is crucial to consider HIV a possible causal factor in CVD occurrence, especially among young patients or individuals without common CVD risk factors.

The COVID-19 pandemic's impact on cardiovascular health behaviors including diet, physical activity, medication adherence, and self-care among people living with HIV (PLWH) remains unknown. Using qualitative analyses, we examined the impact of the COVID-19 pandemic on cardiovascular health behaviors among PLWH. Twenty-four PLWH were enrolled in this multisite study from September to October 2020. Individuals participated in semi-structured telephone interviews that were recorded, transcribed, and coded by 4 independent coders. Codes were adjudicated and analyzed for common themes. Participants were, on average, 59.2 years old (+/-9.4), 75% African American (n = 18) and 71% male (n = 17). The pandemic altered cardiovascular disease health behaviors. PLWH changed diet based on stay-at-home orders and food access. Alterations in physical activity included transitioning from gym and group class exercise to home-based exercise. Antiretroviral adherence was maintained, even when other health behaviors wavered, suggesting resilience in PLWH that may be harnessed to maintain other health behaviors.