Journal of Medical Virology最新文献

While previous studies have primarily focused on post-acute sequelae of COVID-19, the long-term effects of SARS-CoV-2 infection on alopecia areata (AA) among individuals with mental illness remain underexplored. Thus, this study aimed to address this gap by examining the association between post-acute sequelae of COVID-19 and AA, with a specific focus on individuals with mental illness. This study utilized bi-national, large-scale, and population-based cohorts of individuals with pre-existing mental illness: a Korean nationwide cohort (K-COV-N cohort; main cohort; total n = 3 248 448) and a Japanese claims-based cohort (JMDC cohort; replication cohort; total n = 696 332). The outcome focused on the new onset of AA following 30 days after SARS-CoV-2 infection, defined using ICD-10 codes L63. Using a propensity score-based overlap weighted algorithm, the adjusted hazard ratio (aHR) for AA following COVID-19 was calculated for individuals with mental illness. In the main cohort, the risk of AA as post-acute sequelae of COVID-19 was identified among individuals with mental illness (aHR, 1.32 [95% CI, 1.23–1.43]). The risk was significant for mild mental illness (aHR, 1.33 [95% CI, 1.24–1.44]) and within 6 months postinfection (aHR, 1.48 [95% CI, 1.35–1.63]). Similar findings were observed in the replication cohort. In conclusion, among individuals with mental illness, the risk of post-acute sequelae of COVID-19 on AA was elevated—particularly in those with mild mental illness—though this risk decreased over time. Our findings highlight the importance of early screening, integrated care, and equitable healthcare access for managing post-acute sequelae of COVID-19.

Angiogenesis plays a crucial role in the development of HBV-related hepatocellular carcinoma (HCC). VEGFA is a key angiogenic factor, and while its transcriptional regulation by HBV has been extensively studied, its posttranscriptional regulation by HBV remains poorly understood. Building on our previous findings that delineated an RBM15/YTHDF2/IGF2BP3 regulatory axis in m6A-mediated RNA metabolism in HCC, this study further explores the posttranscriptional regulation of VEGFA by HBV. By MeRIP-qPCR and integrating MeRIP-seq data, we discovered that HBV enhances m6A methylation of VEGFA mRNA. Comprehensive cellular and molecular biology experiments demonstrated that HBV induces the upregulation of IGF2BP3, which serves as a key “reader” that recognizes and stabilizes VEGFA mRNA in an m6A methylation-dependent manner. This stabilization leads to elevated VEGFA expression, promoting enhanced cellular functions such as HUVEC migration and tube formation. Furthermore, in an HBV-associated HCC xenograft model, IGF2BP3 knockdown resulted in decreased VEGFA expression and inhibited tumor growth. This study expands our understanding of HBV-driven angiogenesis and identifies the IGF2BP3-VEGFA axis as a potential therapeutic target for antiangiogenic strategies in HBV-related HCC.

Severe fever with thrombocytopenia syndrome virus (SFTSV) presents an emerging public threat due to its high mortality rate and ever-expanding geographic distribution. However, characterization of SFTSV infection pathogenesis and immunological impact at single-cell level remains underexplored. Here, we employ single-cell transcriptome-wide sequencing in peripheral blood mononuclear cells (PBMCs) from hospitalized SFTSV-infected patients to map the immune landscape across acute and convalescent stages of infection. The results reveal significant alterations in immune cell compositions, along with profound disruption in intercellular crosstalk. B cells and neutrophils appear to be the primary target for SFTSV infection besides monocytes, as evidenced by heightened virus-related pathways in these two cell types during the acute phase. In addition, SFTSV infection induces a substantial inflammatory response, which were prominently reflected in monocytes and neutrophils. These data illustrate the complex immune remodeling and inflammatory cascades triggered by SFTSV, with a particular focus on its effects on B cells and neutrophils, bringing novel insights into future therapeutic developments.

Cellular immune responses are crucial in determining outcomes of the hepatitis B virus (HBV) infection. Ineffective immune responses enable persistent HBV infection and contribute to progressive liver disease. Understanding the mechanisms underlying immunological HBV tolerance and restoring functional adaptive immune responses is essential for successful chronic hepatitis B (CHB) treatment. This study examined the dysregulated immune responses and immunopathological cell states associated with CHB using single-cell RNA sequencing of peripheral blood mononuclear cells to investigate immune cell composition and transcriptional differences between patients with CHB and healthy donors. Phenotypic alterations in the lymphoid and myeloid compartments were observed following HBV infection. T cell immune profiling in patients with CHB showed enrichment of exhausted CD8+ T cells, impaired cytotoxicity of effector CD8+ T cells, and increased regulatory T cell (Treg) suppressive activity. Immature neutrophils and a unique CD14+ monocyte subset (myeloid-derived suppressor cells) exhibited potent immunosuppressive abilities. A novel population of CD14+CD163+VSIG4+ M2-like macrophages with immunosuppressive and anti-inflammatory phenotypes was enriched in a patient with severe CHB and liver failure, indicating a potential contribution to dysfunctional immune responses. Our study demonstrated immune exhaustion and evasion in chronic HBV infection, elucidating its immunopathological features and suggesting new therapeutic strategies for immune-mediated disorders and unresolved chronic HBV infection.

Estimating the prognosis of people with newly diagnosed AIDS-related diffuse large B-cell lymphoma (AR-DLBCL) is challenging. We did a prospective, multicenter cohort study using data from 306 consecutive subjects, including training cohort (N = 215) and external validation cohorts (N = 91), to develop and validate a visual nomogram, termed the ARDPI model. Seven co-variates were independently correlated with survival, including age, LMR, CD5, blood EBV-DNA copy number, CD4/CD8, CNS involvement, and anti-HIV therapy (ART), were used to develop the ARDPI model. AUROCs of the model for 1-, 3-, and 5-year survivals were 0.80 (95% CI: 0.72, 0.88), 0.78 (0.69, 0.87), and 0.77 (0.63, 0.91) in the training cohort and 0.85 (0.75, 0.95), 0.80 (0.66, 0.94), and 0.79 (0.61, 0.99) in the external validation cohort. The prediction accuracy of the ARDPI model was better compared with the IPI and NCCN-IPI models. Using the ARDPI model, we identified three risk cohorts with 3-year survivals of 88% (79, 98%), 35% (23, 54%), and 23% (12, 45%) in the training cohort (p < 0.001) and 93% (80, 100%), 46% (27, 78%), and 17% (5, 47%) in the external validation cohort (p < 0.001). The ARDPI accurately predicts the survival of newly diagnosed persons with AR-DLBCL and has clinical benefits. Accuracy is better compared with the IPI and NCCN-IPI prediction models. We also developed a web server to facilitate using our model.