Plain Language SummaryHIV care works best when people can continue testing, treatment, follow-up, and support without interruption. However, people affected by conflict, displacement, migration, and fragile health systems often face serious barriers to HIV services. When people are forced to move, they may lose access to clinics, medicines, health records, laboratory tests, and trusted health workers. This can interrupt antiretroviral treatment, delay viral load monitoring, and increase the risk that people living with HIV are left behind. This letter argues that the global goal of ending AIDS by 2030 should not be measured only by national averages or overall treatment targets. It should also ask whether refugees, internally displaced persons, migrants, mobile populations, and people living in insecure areas can continue HIV prevention, treatment, and care. The letter proposes that countries and donors should include crisis-affected populations in HIV plans, provide emergency antiretroviral medicine refills, use portable health records, strengthen cross-border referrals, pre-position HIV supplies in high-risk areas, and support community-led services. Ending AIDS should mean that people are not excluded from care because they live through conflict, displacement, or health-system disruption.

Despite effective antiretroviral therapy, people living with human immunodeficiency virus (HIV) (PLWH) remain at a higher risk of developing Hodgkin lymphoma (HL). Further, survival disparities persist despite similar treatment recommendations. Herein, we present a global retrospective cohort study including data of adult (≥18 years) diagnosed with HL between 2015 and 2025 from the TriNetX database to evaluate the survival outcomes of Hodgkin lymphoma in HIV-infected versus non-HIV-infected patients and analyze the associated risk factors. Patients were stratified according to HIV status and matched 1:1 for age, sex, race, and comorbidities. Overall survival (OS) was analyzed using Kaplan-Meier and Cox proportional hazards models. A total of 927 matched HIV-infected and non-HIV-infected patients were included. Overall, HIV-positive status was associated with significantly inferior OS (HR 1.42; 95% CI 1.10-1.84; p = 0.033). Among PLWH, cerebrovascular disease, hepatitis C virus infection, and chronic kidney disease independently predicted increased mortality. In a matched subgroup of patients treated with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) chemotherapy (n = 154 per group), OS did not differ significantly between HIV-positive and HIV-negative groups (HR 1.37; 95% CI 0.73-2.56; p = 0.247). In conclusion, HIV-infected patients with HL experienced worse OS compared with non-HIV-infected individuals, but the outcomes were comparable when treated with ABVD chemotherapy, highlighting the importance of optimal treatment delivery and comorbidity management in PLWH.

Hepatitis B virus (HBV) infection remains a major concern among people living with HIV (PLWH), particularly in high-endemic settings such as Vietnam. The study evaluated the serological and molecular characteristics of HBV among PLWH receiving antiretroviral therapy (ART) in southern Vietnam. A cross-sectional study was conducted among 316 HIV-infected patients receiving ART. Serological markers (HBsAg, anti-HBs IgG, and anti-HBc IgG) and HBV DNA were assessed using highly sensitive assays, and the Pre-S1/Pre-S2/S regions were sequenced for genotype and mutation analysis. Associations were evaluated using appropriate statistical methods. HBV DNA was detected in 32.6% of the patients, whereas HBsAg was present in only 16.1%. The most common serological profile was susceptibility (36.4%), followed by occult HBV infection (OBI) (17.4%), including 6.6% with completely seronegative OBI, and chronic HBV (CHB) (15.8%). Males and older individuals showed a significantly higher risk of CHB (adjusted odds ratio [aOR] = 2.58 and aOR = 1.87, respectively). Genotype B predominated (78.4%) overall, but genotype C was significantly more frequent in OBI than in CHB patients (31.5% vs. 8.3%, p = 0.008). Moreover, the burden of surface S gene escape mutations was significantly higher in the OBI group (p = 0.023). The LASSO model showed a moderate discriminatory ability for predicting OBI status (Area Under the Receiver Operating Characteristic [ROC] Curve [AUC] = 0.76). Lamivudine-associated resistance (rtM204I/V) was the most common RT mutation detected in the overlapping RT/S region. HIV-infected individuals in southern Vietnam face a burden of both CHB and OBI, including a high proportion of seronegative OBI. The presence of seronegative OBI further supports the risk of underdiagnosis when relying only on standard serological markers, and reflects the need for integrated strategies combining highly sensitive serological assays with molecular diagnostics to improve HBV detection among high-risk populations.

Antiretroviral therapy (ART) has proven effective in suppressing HIV-1 replication, but further development of HIV-1 inhibitors is continually driven by the challenge of drug resistance and viral adaptation. The HIV-1 capsid is a promising target for treatment due to its high sequence conservation as well as its crucial role in the viral life cycle. Recently, we have developed a novel capsid-targeting biologic that prevents HIV-1 replication by efficient degradation of newly synthesized capsid. Here, we have investigated the sensitivity to viral escape as well as the breadth of this biologic against HIV-1 subtypes. The capsid-targeting biologic efficiently blocked replication of different primary HIV-1 isolates, and continuous exposure of these viruses to the biologic resulted in viral breakthrough of two out of ten primary HIV-1 isolates tested. Notably, the breakthrough variants did not have amino acid changes in the nanobody epitope but primarily in the matrix region. The breakthrough variants remained sensitive to the biologic albeit to a lesser extent. In the absence of the biologic, breakthrough variants showed increased replication kinetics when compared to their parental virus, suggesting that adaption to the biologic is likely due to the increased viral production and that the target area of the biologic is too conserved for actual escape. This is further underscored by the broad specificity of the biologic as importantly the biologic blocked infection of different HIV-1 subtypes that occur worldwide (A, B, C, D, CRF01_AE, CRF02_AG). These results demonstrate the broad neutralization potential of anti-capsid biologics with a high barrier to resistance, making capsid-targeting inhibitors important for novel antiretroviral drug strategies worldwide.

This study investigated the impact of human immunodeficiency virus (HIV) infection and combination antiretroviral therapy (cART) on adipokine concentrations, which are bioactive molecules secreted by adipose tissue and involved in the regulation of metabolism and inflammation. Alterations in adipokine levels may contribute to the metabolic disturbances observed in people living with HIV. The analyzed adipokine panel included resistin, visfatin, chemerin, angiopoietin-like protein 2 (ANGPTL2), lipocalin-2 (LCN2), Wnt family member 5A (Wnt5a), adiponectin, omentin, vaspin, secreted frizzled-related protein 5 (SFRP5), and apelin. Blood samples were collected from people living with HIV and HIV-negative control participants. Adipokine concentrations were measured using an enzyme-linked immunosorbent assay (ELISA). Patients were further stratified according to their cART regimen, including either protease inhibitor (PI)-based or integrase strand transfer inhibitor (INSTI)-based therapy. Plasma concentrations of ANGPTL2 and vaspin were significantly higher, whereas concentrations of visfatin, SFRP5, and adiponectin were significantly lower in HIV-infected patients compared with controls. Comparison of patients receiving INSTI- or PI-based regimens with the control group revealed significant differences in visfatin, SFRP5, and adiponectin concentrations. Notably, adiponectin concentrations were significantly lower in the INSTI-treated subgroup than in patients receiving PI-based therapy. These findings suggest that five of the examined adipokines may be associated with HIV infection and cART exposure, potentially contributing to the development of metabolic disturbances in this population. Further studies involving larger cohorts of individuals with HIV receiving long-term cART are required to better elucidate the relationship between adipokine alterations and the risk of treatment-related metabolic complications.

During HIV infection, the immune system initiates an immune response to control the viremia. In this in vitro study, we investigated the immunomodulatory and anti-HIV potential of a traditional medicine formulation, Product Nkabinde (PN). A freeze-dried extract of PN was used to determine cytotoxicity in MT4 cells. Non-cytotoxic doses were used to evaluate the immunomodulatory and anti-HIV effects of PN using neutralization, prophylactic and treatment approaches. Post-treatment, cytokine quantification and p24 detection were performed. In the neutralization strategy, PN restored IL-1α (p = 0.0389) and IL-10 (p = 0.0443) to levels of uninfected cells. It also reduced HIV-induced elevations in IL-8 (p = 0.035), IP-10 (p = 0.0886), and MCP-1 (p = 0.0733) compared to HIV-infected cells. In the prophylactic approach, HIV infection upregulated IL-1α (p = 0.676), which was suppressed by PN. In the treatment strategy, PN reversed the elevated levels of IL-1α (p = 0.049). IL-10 was fully restored by PN to levels of uninfected cells. In all strategies, PN induced a significant and dose-dependent decrease in HIV replication. These findings demonstrate that PN exerts potent immunomodulatory effects all strategies used by reversing HIV-induced cytokine dysregulation, thereby inducing significant anti-HIV effects.

Despite the success of modern antiretroviral therapy in achieving virological suppression, people living with HIV face an elevated risk of cardiovascular diseases, particularly heart failure with preserved ejection fraction. This study evaluates the cardiometabolic phenotype and functional capacity in a Romanian HIV cohort to delineate the metabolic footprint of chronic infection. In this cross-sectional study based on prospectively collected, protocol-driven phenotyping, we evaluated 50 consecutive outpatients from a university-affiliated infectious diseases clinic in Timisoara. Eligibility strictly required clinical stability and sustained virological suppression (plasma HIV-RNA < 50 copies/mL for ≥12 months). The analysis revealed widespread metabolic dysregulation, with 52% exhibiting excess weight and 64% showing atherogenic dyslipidemia. Integrase strand transfer inhibitor-based regimens were significantly correlated with an increased body mass index (p = 0.034) and elevated LDL cholesterol (aOR = 2.4, 95% CI [1.18-4.95], p = 0.022). Furthermore, we observed a pronounced metabolic age gap (+4.5 ± 2.8 years), defined as the deviation of bioimpedance-estimated metabolic age from the patients' chronological age. This gap (p = 0.028), alongside historical immunodeficiency indicated by a low nadir CD4+ count (aOR = 0.998, 95% CI [0.991-0.999], p = 0.021), strongly predicted exercise intolerance, independent of current immune reconstruction. Sarcopenic obesity (present in 18% of the cohort) and an elevated triglycerides-to-HDL ratio (aOR = 2.14, 95% CI [1.15-3.98], p = 0.016) emerged as robust independent negative predictors of functional capacity. Additionally, subclinical myocardial remodeling, evidenced by impaired Global Longitudinal Strain, significantly predicted reduced aerobic capacity (aOR = 0.72, 95% CI [0.58-0.89], p = 0.003). Consequently, contemporary HIV management must transition beyond virological control to integrated cardiometabolic screening. Utilizing cardiopulmonary exercise testing, echocardiography, and metabolic biomarkers is critical for the early identification of subclinical "functional HIV-associated frailty" and mitigating the trajectory toward overt cardiovascular diseases.