Antiretroviral therapy is critical for preventing perinatal HIV transmission during pregnancy; however, access is shaped by complex structural factors, including access to prenatal care, insurance status and provincial drug-coverage policies. Despite its importance, little is known about how out-of-pocket antiretroviral therapy costs during pregnancy differ within and across Canada. We performed a secondary analysis of Quebec data from the Canadian Perinatal HIV Surveillance Program collected between 2019 and 2023, which included 225 pregnant women and pregnant people living with HIV. Out-of-pocket antiretroviral therapy costs were estimated using insurance information, medication prices, and provincial drug formularies. Additionally, we modelled hypothetical case scenarios to examine how antiretroviral therapy costs during pregnancy differed based on income level and province of residence. In the Quebec cohort, out-of-pocket antiretroviral therapy costs during pregnancy varied substantially by insurance coverage. Individuals without insurance faced median costs in pregnancy nearly 10 times higher (CAD $9380) than those with public (CAD $934) or private insurance (CAD $1196). Those insured under the Interim Federal Health Program incurred no costs (CAD $0). Simulated scenarios across provinces and territories revealed further disparities, with some jurisdictions providing full public coverage while others required out-of-pocket payments up to CAD $4296. Out-of-pocket costs for antiretroviral therapy during pregnancy remain high and inequitably distributed in Canada, with uninsured individuals facing the greatest burden in Quebec. These findings highlight the need for policy reforms to ensure free and equitable access to antiretroviral therapy during pregnancy, regardless of insurance coverage.

Hyperlipidemia and associated risk factors among people living with HIV on antiretroviral therapy: a retrospective cohort study from Eastern China.

HIV controllers are a heterogenous population of people living with HIV who control viral replication without antiretroviral therapy. The purpose of this review is to summarize potential mechanisms of control and to highlight how these can be used in HIV cure strategies. Several recent studies have identified potent HIV-specific CD8 + T cell responses in posttreatment controllers who controlled viral replication after the discontinuation of antiretroviral therapy and postintervention controllers who achieved control after receiving broadly neutralizing antibodies alone or in conjunction with other immune modulators before antiretroviral therapy was discontinued. Other studies have implicated autologous neutralizing antibodies as a correlate of protection in both groups of controllers. The early initiation of antiretroviral therapy coupled with strategies to enhance HIV-specific CD8 + T cell and autologous neutralizing antibodies may lead to a higher incidence of posttreatment control.

Approaches to strengthen Data-to-Care (D2C) models are needed. We tested an insurance-based D2C prescription model (D2C-Rx), which used antiretroviral therapy (ART) prescription claims to identify people with HIV who fail to fill ART prescriptions in a timely manner and to provide ART adherence support. The Antiretroviral Improvement among Medicaid EnrolleeS (AIMS) study was the first trial of an insurance-based D2C-Rx program. We describe AIMS study enrollment, focusing on patient-participants in the AIMS program arm. Virginia, United States. AIMS used Virginia Medicaid claims and HIV surveillance data to identify Medicaid enrollees with HIV who were without an ART prescription and their providers; study staff then provided targeted adherence support. The target patient-participant sample size was 1000. The outcome of interest was HIV viral suppression. The study encountered difficulty recruiting patient-participants. Low enrollment prompted major changes to the protocol, including revisions to study design, eligibility criteria, and recruitment methods. These changes were unsuccessful. The trial was terminated because of low patient-participant enrollment (n = 4). Reasons for low patient-participant enrollment may include phone-based recruitment approach, lengthy identity verification and consent procedures, and lack of participant compensation. Although we aimed to identify people with HIV without a current ART prescription refill, several participants reported having their medications available; this discrepancy suggests issues with unexpected participant behavior (eg, stockpiling) or timeliness and accuracy of prescription claims data. Future insurance-based D2C-Rx interventions should account for these challenges, be tailored to context, and be nimble enough to pivot to alternative recruitment methods when needed.

Past studies of hepatitis B vaccines in people with HIV (PWH) have shown mixed results about improving responses with increases in dose or dose frequency, leading to inconsistent guidelines and practice. We examined vaccine series completion and revaccinations in PWH lacking a seroprotective response. Hepatitis B vaccination histories were evaluated as a retrospective study in 561 participants of A5379 trial (NCT04193189). Individuals in 41 sites in Africa, Asia, South America, and the United States qualified for the trial with antibody titers below the seroprotective level (<10 mIU/mL) despite past hepatitis B vaccinations. The primary measure of interest was the number of vaccines in the past vaccination records. Of the 1098 trial candidates, 561 (51%) did not have seroprotective titers at the time of screening and enrolled in A5379. Median age at the time of screening was 46 years (18-70 years), which varied across the regions: the lowest in Africa and the highest in the United States. The number of past hepatitis B vaccines varied widely across and within geographic regions. Twenty-four percent of the participants received ≥4 doses, up to 12, yet did not have seroprotective antibody titers. Regardless of past vaccine records, antibody titers should be checked in PWH for revaccination needs. The recently approved long-acting and injectable antiretroviral treatment (ART) lacks protective effect against HBV, unlike tenofovir-based ART. As the long-acting ART becomes more widely used, we recommend reassessing serologies and offering the recommended CpG-adjuvanted vaccine series with promising response durability to individuals without seroprotection.

Do HIV-positive patients achieve successful outcomes in elective orthognathic osteotomies?: A case series.

HIV disease progression following WHO treat all guideline adoption among people enrolled in HIV care in Central Africa: A multistate analysis.

Elite controllers, rare individuals who maintain undetectable HIV-1 viremia without antiretroviral therapy, represent a human model of a functional cure. Understanding the host genetic factors that enable this spontaneous viral control is a key goal of HIV-1 research. This review synthesizes recent findings that are challenging and expanding the classic, human leucocyte antigen (HLA)-centric view of elite control. While the dominant association of specific HLA class I alleles (e.g., HLA-B*57, HLA-B*27) with low set-point viral load remains the cornerstone of the field, recent research has highlighted three emerging themes. First, the discovery of a large-effect, Africa-specific genetic association near the CHD1L locus has underscored the critical importance of studying genetically diverse populations. Second, novel approaches have highlighted a multilayered cellular response to HIV-1, suggesting more complex mechanisms of control beyond genetics alone. Third, a central paradox has emerged: the host genetic factors that strongly impact viral load do not show any association with the size or decay rate of the latent viral reservoir in treated individuals, complicating the path from "control" to "cure." The genetic architecture of HIV-1 elite control is more complex than previously appreciated. The field has moved beyond HLA to uncover new, ancestry-specific pathways, explore multiple biological variables, and confront the critical disconnect between controlling viremia and eliminating the latent reservoir.

Although ART suppresses HIV-1 viral loads to undetectable levels and frequently enables a near-normal life expectancy for persons living with HIV, a reservoir of infected cells persists lifelong and cannot be eliminated with currently available therapeutic strategies. This review summarizes recent discoveries to elucidate the underlying causes of HIV-1 persistence despite antiretroviral therapy and offers insights for future interventions. Recent advances in proviral sequencing, chromosomal integration site mapping, clonal cell tracking, single-cell multiomics, and spatial transcriptomic profiling reveal that HIV-1 persistence is not merely due to viral latency. Instead, it is also sustained by clonal expansion, cell-intrinsic survival programs, and immune-evasion properties of reservoir cells, as well as by the protective microenvironments found in specific tissue sanctuaries. While no single factor is identified as the sole driver of persistence, these findings collectively reshape and expand our understanding of HIV-1 reservoirs and the mechanisms underlying viral persistence. HIV-1 persists through a multilayered network in which viral latency, clonal proliferation, cell-intrinsic survival and immune-evasion programs, and the biology of tissue sanctuaries act in concert to sustain the viral reservoir. This interconnected architecture-rather than any single mechanism-constitutes the fundamental basis of HIV-1 persistence.

People with HIV (PWH) using antiretroviral therapy are at increased risk to develop cardiovascular diseases (CVD). We hypothesized that residual viremia (RV; unquantifiable low, but detectable viral load) increases CVD risk. We enrolled 1895 virally suppressed PWH and compared CVD incidence in participants with and without RV. Extensive multi-omics characterization was performed. Incident CVD was registered after 2-year follow-up and adjusted odds ratios (aOR) calculated accounting for classical CVD risk factors. The numbers of expected and actual CVD events were compared using CVD risk scores. RV, detected in one-third of participants, strongly increased the risk of developing a first cardiovascular event (3.1% vs 1.2%, aOR 2.8,p=0.004). Participants with RV experienced twice the number of events predicted by the SCORE2 riskmodel. The association between RV and CVD was not driven by inflammation, immune activation, gut barrier dysfunction, or lipometabolic perturbations. Residual viremia independently associated with CVD development, highlighting the need for tailored prevention and examination of novel intervention strategies.

Saliva is a non-invasive way to study oral viruses, but we lack specific data on Human Polyomaviruses (HPyVs) and Herpesviruses (HHVs) in HIV-positive patients. Currently, the co-infection patterns and viral loads in this population are not well understood compared to healthy individuals. Our study fills this gap by analyzing these viral profiles and microRNAs in saliva. This work helps establish saliva as a dependable diagnostic method for these infections. A cross-sectional study assessed the prevalence of six Human Polyomaviruses (HPyVs) and five Human Herpesviruses (HHVs) in saliva samples collected from two cohorts: 20 HIV-positive individuals undergoing antiretroviral therapy (ART) and 37 HIV-negative subjects. Molecular analyses were performed using quantitative PCR (Q-PCR), with absolute quantification of viral loads and detection of JCPyV and MCPyV microRNAs (miRNAs). The results showed higher overall prevalence of HPyVs (60 % vs. 32.4 %) and HHVs (75 % vs. 51.3 %) in the HIV-positive group compared to the HIV-negative group. MCPyV and EBV were the most frequently detected viruses in both cohorts, but their mean loads were significantly higher in the HIV-positive group. Viral co-infections were more common among HIV-positive individuals (40.0 % vs. 32.4 %), with a predominance of HPyV/HHV co-infections. Notably, HPyV miRNAs were detected also in samples negative for the corresponding viral genomes. Our findings confirm saliva's utility for detecting viral co-infections and highlight the need to determine if oral HPyVs and HHVs act as bystanders or pathogens in HIV-positive patients.

Targeting α7nAChR-driven brain endothelial pyroptosis mitigates HIV-1 gp120-induced blood-brain barrier breakdown.

HIV diagnosis following psychiatric hospitalization among a large cohort of privately-insured people in the United States, 2003-2024.

Effects of doxycycline post-exposure prophylaxis on bacterial sexually transmitted infections and antiretroviral therapy adherence among adolescents and young adults living with HIV.

A computational approach for classification of HIV drug resistance based on the self-consistent extreme classifier.

Evaluation of two bioinformatic algorithms for the interpretation of HIV-1 drug resistance and subtyping in Cameroon: Translational application for ART optimization in low-and middle-income countries.

Objectives. To estimate the increase in HIV infections in 11 US states if Ryan White services are interrupted or ended. Methods. We applied a population-level model of HIV transmission to 11 states. We represented the proportion of people with HIV receiving Ryan White AIDS drug assistance, outpatient health services, or support services, and simulated a loss of suppression in each category if services permanently end or return after delays of 1.5 or 3.5 years. Results. Cessation of Ryan White services in 2025 was projected to result in 69 695 additional infections from 2025 to 2030 (95% credible interval [CrI] = 18 943, 123 628), 68% more (95% CrI = 18%, 118%) than if Ryan White were continued. Temporary interruptions of 1.5 and 3.5 years resulted in 26 951 (95% CrI = 7341, 47 534) and 53 594 (95% CrI = 14 645, 94 860) additional infections, respectively. Excess infections varied across states, from a 45% increase in Texas to 126% in Missouri. Conclusions. Projected increases in HIV infections because of disruptions of Ryan White services threaten the progress made in curtailing the US HIV epidemic, illustrating the critical role Ryan White plays in preventing HIV transmission. (Am J Public Health. 2026;116(5):732-735. https://doi.org/10.2105/AJPH.2025.308409).

The Ryan White HIV/AIDS Program (RW) serves as a critical safety net for low-income and underinsured people living with HIV (PWH). We assessed the relationship between the utilization of comprehensive RW services (core, support, and AIDS Drug Assistance Program) and sustained HIV viral suppression. Despite the expansion of Medicaid under the Affordable Care Act, South Carolina failed to expand its eligibility, leaving many vulnerable PWH without coverage. We used a statewide cohort of PWH to identify epidemiologic trends and develop predictive models to improve clinical HIV and public health services. We analyzed data from 8489 PWH diagnosed in South Carolina (2005-2020) to identify sustained viral suppression (consecutive undetectable viral load tests within a year). We report the descriptive statistics and bivariate associations with sustained viral suppression. Subsequently, using generalized linear mixed modeling, we modeled the relationship between RW service utilization and sustained viral suppression, controlling for key sociodemographic, substance use, mental health, and HIV clinical care variables. Our sample of PWH (n = 8489) was primarily young (18-30 years, 42%), men (75%), Black (71%), urban (83%), and 88.3% achieved sustained viral suppression. RW service utilization was more frequent for core (65%) and support services (53%), whereas only 3% used comprehensive (core, support, and AIDS Drug Assistance Program) services. Our adjusted model revealed that comprehensive utilization significantly increased the odds of sustained viral suppression by 41% (AOR = 1.41, 95% CI = 1.09 to 1.84). Our findings highlight the importance of structural support and comprehensive low-barrier services for achieving HIV progress in a shifting landscape of health care coverage.

A 67-year-old man with long-standing HIV on antiretroviral therapy, type 2 diabetes with polyneuropathy, and hyperlipidemia on statin and fibrate therapy presented with difficulty walking and exercise intolerance. Examination revealed new hamstring weakness superimposed on chronic distal weakness and sensory loss. Initial laboratory testing showed elevated creatine kinase, which persisted despite discontinuation of statin and fibrate therapy. In this article, we review the approach to adult-onset myopathy and explore diagnostic challenges when clinical and diagnostic testing seem discordant, emphasizing a stepwise approach to localization, differential diagnosis, and targeted testing.

Abstract Background Adherence to antiretroviral therapy (ART) during pregnancy is critical for maternal health and the prevention of vertical HIV transmission. In Uganda, where HIV prevalence remains high, pregnant women living with HIV face intersecting structural and psychosocial challenges, including stigma, food insecurity, and limited social support. Although each factor has been linked to ART nonadherence, less is known about how these factors co-occur within individuals and jointly shape vulnerability to nonadherence during pregnancy. Objective This study used latent profile analysis to identify empirically derived psychosocial vulnerability profiles reflecting the co-occurrence of stigma, food insecurity, and limited social support among pregnant women living with HIV in Uganda and examine whether profile membership is associated with ART adherence. Methods We conducted a cross-sectional analysis of 167 pregnant women living with HIV recruited from 6 health facilities in Uganda between June and December 2020. Measures included experienced HIV stigma, internalized HIV stigma, household food insecurity, and interpersonal social support. Latent profile analysis identified psychosocial profiles, and linear regression models assessed associations between profile membership and ART adherence, adjusting for sociodemographic covariates. Results A 2-class solution provided the best model fit (entropy=0.93). The higher-risk profile (75/167, 45.1%) was characterized by increased experienced stigma (mean score 1.97, SE 0.05), higher internalized stigma (mean score 2.66, SE 0.07), severe food insecurity (mean score 7.53, SE 0.20), and lower social support (mean score 2.06, SE 0.04). The lower-risk profile (92/167, 54.9%) showed significantly lower internalized stigma (mean score 2.32, SE 0.04; P &lt;.001), lower experienced stigma (mean score 1.72, SE 0.05; P &lt;.001), minimal food insecurity (mean score 0.82, SE 0.15; P &lt;.001), and slightly higher social support (mean score 2.14, SE 0.04; P &lt;.001). Membership in the higher-risk profile was associated with significantly lower ART adherence compared with membership in the lower-risk profile (B=0.88; β=0.40, 95% CI 0.02-0.78; P =.04). Conclusions Distinct psychosocial profiles are meaningfully associated with ART adherence among pregnant women living with HIV in Uganda. By moving beyond single-risk models, these findings demonstrate the added value of person-centered analytic approaches for identifying subgroups of pregnant women living with HIV exposed to clustered psychosocial and structural vulnerabilities. The findings underscore the need for multicomponent, person-centered interventions that simultaneously address stigma, food insecurity, and limited social support rather than treating these challenges in isolation. Identifying empirically derived vulnerability profiles provides a targeted framework for prioritizing high-risk subgroups and informing contextually appropriate intervention design. Addressing these intersecting vulnerabilities is essential for improving maternal ART adherence and supporting efforts to prevent vertical HIV transmission in high-burden settings.