HIV Medicine最新文献

Objectives: In England, HIV pre-exposure prophylaxis (PrEP) was routinely commissioned at sexual health services from 2020. We compared PrEP use and unmet need among gay, bisexual and other men who have sex with men (GBMSM) in London before (2019) and during (2022) routinely commissioned PrEP and the factors associated with its use.

Methods: Cross-sectional, self-administered surveys were conducted in London commercial venues in 2019 (n = 1408) and 2022/2023 (n = 1090). Anonymous questionnaires collected data on socio-demographic characteristics, sexual behaviours, service engagement and outcomes. PrEP need was defined as condomless anal sex (CAS) in the last 3 months or with HIV-positive/unknown status partners not on HIV treatment in the last year. Multivariable logistic regressions examined factors associated with PrEP use.

Results: Among HIV-negative/unknown GBMSM, current PrEP use more than doubled (19.9% (245/1233) in 2019 to 44.2% (360/814) in 2022 (p < 0.001)), representing 2.7-fold higher odds of PrEP use among GBMSM with identified PrEP need pre- to post-commissioning (aOR: 2.74, 95% CI: 2.13-3.54). Age disparities remained, whereby men aged 40-44 years had higher odds of PrEP use compared to those 18-24 years (aOR: 3.34, 95% CI: 1.93-5.78). Current PrEP users also reported higher healthcare engagement and sexual risk behaviours than those with unmet PrEP need. Meanwhile, unmet PrEP need declined significantly from 67.9% (431/635) in 2019 to 43.8% (212/484) in 2022 (p-value < 0.001).

Conclusions: While routine PrEP commissioning increased PrEP use, age disparities remained, as did high levels of unmet PrEP need among GBMSM in London. This highlights the importance of targeted interventions to achieve equitable PrEP access.

Background: People living with HIV (PLWH) face a higher risk of cardiovascular disease (CVD), with significant sex differences in outcomes. However, it is unclear whether these differences are driven by distinct risk factor profiles or by a differential impact of shared risk factors. This study aimed to identify factors associated with CVD among PLWH and to specifically assess for effect modification by sex using a large, diverse nationwide database.

Methods: We utilized data from the All of Us Research Program (AoU). The primary outcome was a composite of coronary artery disease or stroke. We used multivariable logistic regression to identify factors associated with CVD in the overall cohort. To assess for effect modification, we introduced interaction terms between sex and key covariates. Subsequently, sex-stratified analyses were performed to explore these differences.

Results: Among 6464 PLWH (4608 men and 1856 women), women had a higher prevalence of CVD than men (24.8% vs. 21.9%, p = 0.011). We identified significant interaction effects between sex and several key risk factors, including hypertension, unemployment and hyperlipidaemia (p < 0.05 for all). In stratified analyses comparing women to men within these risk groups, the association of hypertension with CVD was substantially stronger in women than in men (adjusted odds ratio [aOR] = 4.928, 95% CI: 2.827-8.586). Similarly, the effects of unemployment and hyperlipidaemia on CVD were more pronounced in women. In fully stratified models, a detectable viral load was a significant risk factor for CVD only among men (aOR = 1.524, 95% CI: 1.130-2.049).

Conclusions: While many traditional and HIV-specific CVD risk factors are shared between men and women living with HIV (WLWH), our findings reveal that the magnitude of their effect is not uniform. The impact of key risk factors, particularly hypertension, is substantially greater in women, suggesting a heightened vulnerability to these exposures. These findings underscore the critical need for sex-specific risk assessments and aggressively tailored prevention strategies for PLWH.

Background: With the widespread use of antiretroviral therapy (ART), life expectancy among people living with human immunodeficiency virus (HIV) infection has significantly increased. However, studies on HIV-associated emphysema, especially those addressing the mechanisms, remain limited. In this study, we analysed transcriptomic data from Gene Expression Omnibus (GEO) to investigate the underlying mechanisms and identify biomarkers of HIV-associated emphysema.

Methods: The gene expression profiling data of HIV infection (GSE76246, peripheral blood samples), emphysema (GSE11906, airway tissue samples) and HIV-associated emphysema (GSE76403, peripheral blood samples) were obtained. We performed differential expression gene (DEG) analysis, functional enrichment analysis, weighted gene co-expression network analysis (WGCNA), protein-protein interaction (PPI) network analysis and random forest modelling to explore the mechanisms and candidate biomarkers of HIV-associated emphysema. The expression of candidate biomarkers was subsequently validated in the comorbidity dataset, and immune cell infiltration was assessed.

Results: We identified genes shared between HIV infection and emphysema and trait-relevant modules. Functional enrichment analysis suggested that persistent immune activation, altered RNA metabolism, protein translation, enhanced oxidative stress responses and potential adverse effects of ART via P450 might contribute to HIV-associated emphysema. PPI network analysis and random forest modelling identified Glutathione-disulphide reductase (GSR) and Carbonyl reductase 1 (CBR1) as candidate biomarkers, which were preliminarily supported by findings from the comorbidity dataset. Immune cell infiltration analyses indicated increased proportions of memory B cells, activated dendritic cells, CD8+ T cells, gamma delta T cells and Tregs, along with decreased levels of resting mast cells and naive CD4+ T cells in HIV-associated emphysema.

Conclusion: Our study suggests possible mechanisms and candidate biomarkers (GSR and CBR1) for HIV-associated emphysema and also provides exploratory insights into potential immune dysregulation in affected patients. However, due to the heterogeneity of tissue sources, limited sample size and the fact that the mechanistic insights were inferred from bioinformatics analyses rather than experimental validation, the cross-tissue relevance of shared genes remains speculative and the immune infiltration findings based on peripheral blood transcriptomes may not fully reflect lung immune composition. Therefore, these findings should be interpreted with caution.

Introduction: People with HIV have an increased risk of cardiovascular disease (CVD). Despite this, commonly used CVD risk scores have been developed for the general population, which may underestimate risk in people with HIV. This study aims to evaluate the concordance of five risk prediction models (SCORE2, REGICOR, REGICOR 3.0, D:A:D reduced and D:A:D full) in a cohort of people with HIV.

Methods: This cross-sectional study enrolled 246 participants aged 18-75 at a single centre in Barcelona, Spain. Demographic, clinical and laboratory data were collected to calculate 10-year CVD risk using each model. Risk categories were compared using a chi-square test followed by a post hoc analysis with Bonferroni's correction for multiple comparisons. Concordance was assessed using Lin's concordance correlation coefficient (CCC), and agreement was evaluated with Bland-Altman analysis.

Results: The risk category distribution differed significantly across models (χ² = 53.6, df = 12; p < 0.001). REGICOR classified most individuals as low-risk (66.2%), whereas REGICOR 3.0 and D:A:D full identified more as very high-risk (44.4% and 41.9%, respectively). Concordance was highest between D:A:D full and reduced (CCC = 0.82), good between SCORE2 and REGICOR (CCC = 0.78) and poor between most HIV-specific and general population models (CCC < 0.5). Bland-Altman analyses revealed systematic bias, particularly between REGICOR and D:A:D full.

Conclusions: Cardiovascular risk scores showed limited concordance and poor interchangeability in people with HIV. The discrepancies between the general population and HIV-specific models highlight the need for validated and HIV-adapted tools to accurately assess CVD risk in this population.