Ping Ma

Background: People living with human immunodeficiency virus (HIV) accounted for a large share of cases during the 2022 multinational mpox outbreak, but whether adverse outcomes are attributable to HIV infection itself or to the degree of immune dysfunction remains uncertain. Methods: We conducted a systematic review and meta-analysis according to PRISMA 2020 and Cochrane methods. PubMed, Embase, and Web of Science were searched from inception through January 31, 2026, with targeted literature updating through May 27, 2026. Observational studies reporting mpox outcomes stratified by HIV status were eligible. The primary outcome was hospitalization. Risk ratios (RRs) were pooled using DerSimonian-Laird random-effects models. Results: Twenty studies were included in the qualitative synthesis and 13 studies comprising 32,685 participants were included in the hospitalization meta-analysis. HIV infection was associated with increased hospitalization risk (RR, 1.40; 95% CI, 1.07–1.85; I ² = 81%). The 95% prediction interval was wide (0.54–3.65), indicating that context, case mix, and hospitalization thresholds influenced observed effects. CD4-stratified evidence was not sufficiently uniform for a valid pooled CD4-specific effect estimate, but available studies consistently indicated that low CD4 count, uncontrolled HIV viremia, and disengagement from HIV care identify the subgroup at greatest risk for hospitalization, severe disease, prolonged infection, and death. Conclusion: Adverse mpox outcomes among people living with HIV are better explained by immune status and HIV disease control than by HIV serostatus alone. CD4-based risk stratification provides a clinically actionable framework for triage, follow-up intensity, antiviral-treatment consideration, and integration of mpox management with HIV care.

Background: Hypertension (HTN) is a frequent comorbidity in people living with Human Immunodeficiency Virus (HIV), yet the shared molecular determinants remain poorly defined. This study aimed to identify diagnostic biomarkers and regulatory networks underlying HIV-HTN comorbidity. Methods: Transcriptomic datasets from HIV (GSE140713) and HTN (GSE236442) cohorts were analyzed to screen differentially expressed genes. Functional enrichment, GSEA, and PPI analyses were performed to uncover shared pathways and hub genes. Immune cell infiltration was evaluated using CIBERSORT. Transcriptional and post-transcriptional regulatory networks were constructed through NetworkAnalyst, miRNet, and starBase. Key genes were validated in peripheral blood samples from healthy individuals, HIV patients, and HIV-HTN patients using qRT-PCR. Results: A total of 109 overlapping genes were identified, converging on cytokine-cytokine receptor interaction, IL-17, and NF-κB pathways. Six hub genes ( FOS, PTGS2, TRMT2A, E2F1, FASN, STAB1 ) were shared across both diseases. Immune deconvolution showed prominent involvement of DC, monocytes, macrophages, NK/NKT cells, and T-cell subsets. qRT-PCR confirmed consistent upregulation of TRMT2A, E2F1, FASN , and STAB1 , and downregulation of FOS and PTGS2 . A putative ceRNA network was constructed, highlighting several candidate regulatory miRNAs and lncRNAs. Conclusion: This integrative analysis suggests potential molecular signatures and immune-related regulatory axes that may contribute to HIV-HTN comorbidity, providing hypothesis-generating leads for biomarker discovery and mechanistic follow-up studies.

Background: Although MDSCs are widely recognized for their immunoinhibitory effects in pathological conditions, their function during HIV infection particularly within the mechanisms underlying incomplete immune recovery remains elusive.Methods: We conducted a cross-sectional study in which 30 healthy controls and 62 HIV-1-infected subjects [31 immunological non-responders (INRs) and 31 immunological responders (IRs)] were selected. The proportion of MDSCs was determined in each category of participants. Using flow cytometry and real-time PCR, immune regulatory molecules (including PD-L1, ARG1, iNOS, IL-10, TGF-β, and IDO) that are relevant for MDSCs activity were quantified. Furthermore, we investigated the impact of the blockade of PD-L1 and TGF-β pathways on MDSCs and their effects on CD4+ T-cells using in vitro functional experiments.Results: PMN-MDSCs are more abundant and are negatively correlated to CD4 counts in HIV-infected individuals. In addition, PMN-MDSCs suppress CD4+ T-cell proliferation and IFN-γ production in INRs. Furthermore, correlations were found between PD-L1 expression on PMN-MDSCs and PD-1+ CD4+ T-cells. TGF-β expression on PMN-MDSCs was likewise enhanced in INRs. Importantly, inhibiting both PD-L1 and TGF-β pathways had a synergistic impact on restoring CD4+ T-cell activity in vitro.Conclusions: PMN-MDSCs expansion inhibits CD4+ T-cell responses. We suggest that targeting PD-L1 and TGF-β pathways together may significantly improve immune recovery in INRs.

Despite the proven virological advantages, there remains some controversy regarding whether first-line integrase strand transfer inhibitors (INSTIs)-based antiretroviral therapy (ART) contributes to reducing mortality of people living with HIV (PLHIV) in clinical practice. Here we report a retrospective study comparing all-cause mortality among PLHIV in China who were on different initial ART regimens (nevirapine, efavirenz, dolutegravir, lopinavir, and others [including darunavir, raltegravie, elvitegravir and rilpivirine]) between 2017 and 2019. A total of 41,018 individuals were included across China, representing 21.3% of newly reported HIV/AIDS cases collectively in the country during this period. Only the differences in all-cause mortality of PLHIV between the efavirenz group and the nevirapine group, the dolutegravir group and the nevirapine group, and the lopinavir group and the nevirapine group, were observed in China. After stratifying the cause of mortality, we found that the differences in mortality between initial ART regimens were mainly observed in AIDS-related mortality.

Studies assessing the gut mucosal immune balance in HIV-infected patients using intestinal samples are scarce. In this study, we used intestinal mucosal specimens from the ileocecal region of seven immunological nonresponders (INRs), nine immunological responders (IRs), and six HIV-negative controls. We investigated T helper 17 (Th17) and T regulatory (Treg) cell counts and their ratio, zonula occludens-1 (ZO-1), intestinal fatty acid-binding protein (I-FABP), tumor necrosis factor-α, CD4⁺ T cell counts, HIV DNA, and cell-associated HIV RNA. The results showed that INRs had lower Th17 and higher Treg cell counts than IR, resulting in a significant difference in the Th17/Treg ratio between IRs and INRs. In addition, INRs had lower ZO-1 and higher I-FABP levels than IRs. The Th17/Treg ratio was positively associated with ZO-1 and negatively associated with I-FABP levels. There was a positive correlation between Th17/Treg ratio and CD4⁺ T cell counts and a negative correlation between the Th17/Treg ratio and HIV DNA in the intestine. Our study suggests that the imbalance of Th17/Treg in the intestine is a characteristic of incomplete immune reconstitution to antiretroviral therapy and is associated with intestinal damage.

Purpose: The genetic diversity and genetic predisposition for drug resistance mutations are the primary features of human immunodeficiency virus type 1 (HIV-1), which could cause the incidence of failure of antiretroviral therapy (ART). This study investigates the distribution of various HIV-1 genotypes and the incidence of pretreatment drug resistance (PDR) in the antiretroviral-naive HIV-1 infected participants in Xi’an, China. Patients and Methods: In this study, a cross-sectional analysis was carried out at the Xi’an Eighth Hospital between January 2020 and December 2021 among newly-diagnosed ART-naive HIV-1 infected participants. A nested PCR technique was used for amplifying the target segment of 1.3 kb present in the pol gene that spanned the reverse transcriptase and the protease regions. HIV-1 genotypes and the PDR-associated mutations were identified using the Stanford HIV Drug Resistance Database. Results: A total of 317 pol gene sequences were retrieved, amplified, and sequenced. The circulating recombinant form (CRF), CRF07_BC (51.7%) was seen to be the most prevalent HIV-1 genotype, followed by other genotypes like CRF01_AE (25.9%), B (14.2%), and CRF55_01B (4.7%). PDR was found in 18.3% of the population. The PDR mutation frequency in the non-nucleoside reverse transcriptase inhibitor (NNRTI) (16.1%) was significantly higher compared to that of the nucleoside reverse transcriptase inhibitor (NRTI) (4.4%) and the protease inhibitor (0.9%). V179D/E (both were 4.4%) was seen to be the most predominant type of NNRTI mutation. K65R and M184V (1.3%) were the most frequent NRTI-associated mutations. About half (48.3%) of the sequenced HIV-1 strains that had mutations could show a potential low-level NNRTI resistance owing to V179D/E. Multivariate regression analysis revealed one PDR mutation associated with subtype CRF01_AE (p=0.002) and CRF55_01B (p< 0.001) as a higher risk mutation. Conclusion: Diverse and complex HIV-1 genotypes are distributed in Xi’an, China. Considering new evidence, it is necessary to screen for baseline HIV-1 drug resistance among the newly-diagnosed HIV-1 individuals.