VIROLOGICA SINICA中国病毒学
VIROLOGICA SINICA(英文缩写 VIROL SIN),ISSN 1674-0769,eISSN 1995-820X,中文译名:中国病毒学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.947 | Q2 |
| 2022 | 5.500 | Q1 |
| 2023 | 4.300 | Q2 |
| 2024 | 4.000 | Q1 |
| 2025 | 4.700 | Q1 |
VIROLOGICA SINICA 最新收录文献
-
2. SFTSV exploits PPM1K to inhibit apoptosis through the Bcl-2/BAX/Caspase-3 axis for efficient replication.
PMID:日期:2026-09-24SFTSV (Severe fever with thrombocytopenia syndrome virus) causes severe febrile illness with high case fatality rates and poses a growing public health threat, while the molecular basis by which it subverts host survival pathways remains poorly understood. In this study, transcriptomic profiling identified PPM1K as a prominently induced host factor in SFTSV-infected THP-1-derived macrophages. We further demonstrate that SFTSV infection promotes endoplasmic reticulum-mitochondria coupling, enabling the viral glycoprotein Gc to interact with mitochondrial PPM1K and enhance its expression at both transcriptional and protein levels. Mechanistically, the S248 residue of PPM1K is required for its dephosphorylation of Bcl-2, thereby decreasing Bcl-2 ubiquitination and stabilizing its anti-apoptotic activity, which ultimately suppresses the BAX-Caspase-3 signaling cascade. This anti-apoptotic remodeling markedly limits apoptosis in infected cells and facilitates efficient SFTSV replication. These findings uncover a previously unrecognized viral strategy in which SFTSV hijacks host PPM1K-dependent mitochondrial signaling to evade apoptosis and promote replication.
-
3. Establishment of a Tandem Dimeric Replication System for Torque Teno Virus In Vitro.
PMID:日期:2026-09-23该文献暂无摘要。
-
4. Subcutaneous immunization with replication-competent live influenza virus confers durable protective immunity without respiratory pathology in mice.
PMID:日期:2026-09-21Current influenza vaccination strategies are constrained by the trade-off between the safety of inactivated platforms and the immunogenic potency of live attenuated vaccines. Here, we provide a comprehensive demonstration that subcutaneous (SC) immunization with a non-attenuated, replication-competent live influenza A virus (LIV) decouples immunogenicity from pathogenicity. Using a murine model, we show that a single high-dose SC immunization of A/Puerto Rico/8/34 (H1N1) elicited sterile pulmonary immunity against lethal challenge, significantly outperforming intramuscular delivery and inactivated vaccines. Biodistribution analysis confirms viral replication is transient (< 7 days) and strictly restricted to the injection site and draining lymph nodes, with no systemic dissemination to the lungs or central nervous system. Mechanistically, single-cell transcriptomics reveal that SC delivery triggers a localized type I interferon "firewall" that transitions into a robust germinal center (GC) reaction, fostering extensive plasma cell differentiation and superior memory B cell formation compared to phosphate-buffered saline (PBS)-treated controls. This regimen conferred 100% protection at 277 days post-immunization. Together, these findings establish peripheral LIV administration as a high-potency paradigm for next-generation rapid-response vaccines.
-
5. EHD4 facilitates Zika virus infection by regulating extracellular vesicle-associated viral release and cell attachment.
PMID:日期:2026-09-18Extracellular vesicles (EVs) and other extracellular membrane-associated particles can contribute to viral dissemination; however, the host factors that regulate the composition and infectivity of EV-associated viral material remain incompletely understood. Here, comparative proteomic profiling identified Eps15 homology domain-containing protein 4 (EHD4) as a candidate host factor enriched in EV/virion-containing preparations from Zika virus (ZIKV)-infected Vero cells. Genetic ablation of EHD4 in HeLa cells impaired the propagation of ZIKV, Japanese encephalitis virus, and dengue virus serotype 2, whereas EHD4 re-expression restored viral propagation. In ZIKV-infected EHD4-knockout (KO) cells, a greater proportion of extracellular viral RNA was recovered in EV-enriched fractions than in wild-type (WT) cells. However, viral material recovered from KO-derived EV-enriched fractions exhibited reduced cell-binding activity and lower infectivity. Partial disruption of membrane integrity attenuated the difference in infectivity between WT- and KO-derived preparations, suggesting that membrane-associated components contribute to the functional properties of the associated viral material. ZIKV replicon assays showed no major effect of EHD4 on viral RNA replication. Immunofluorescence showed partial colocalization of EHD4 with CD63-positive compartments and ZIKV envelope protein. Transmission electron microscopy revealed that EHD4 loss did not affect multivesicular body (MVB) formation, but virus-like particles were readily observed in MVB lumens of WT cells and rarely in KO cells, suggesting that EHD4 promotes viral sorting into MVB luminal vesicles. Quantitative proteomic analysis further identified reduced abundance of a subset of membrane-associated proteins in KO-derived EV-enriched fractions. Collectively, these findings identify EHD4 as a host factor that influences the extracellular partitioning, composition, and infectivity of flaviviral material recovered in EV-enriched fractions. The molecular mechanisms underlying these effects remain to be defined.
-
6. Flavivirus NS1 possesses NTPase and RNA helix unwinding activities.
PMID:日期:2026-09-17Flaviviruses are a group of arthropod-borne positive-sense RNA viruses, including Zika virus (ZIKV), dengue virus 2 (DENV2) and Japanese encephalitis virus (JEV). For RNA viruses, RNA helicases play critical roles in viral replication by unwinding double-stranded RNA intermediates generated in viral life cycles by remodelling viral RNA structures. Here, we report that NS1 proteins from ZIKV, DENV2 and JEV, possesse NTPase and RNA helix unwinding activities. ZIKV NS1 unwinds dsRNA in an NTP-dependent manner with 5'→3' directionality, and its unwinding activity is broad-spectrum, targeting dsRNA, dsDNA and RNA/DNA hybrids. Moreover, both DENV2 and JEV NS1 also display NTPase and helicase activities, but they differ in substrate preference and directionality: JEV NS1 unwinds in the 5'→3' direction like ZIKV NS1, whereas DENV2 NS1 unwinds only shorter duplexes and shows 3'→5' directionality. Mutagenesis identified the basic residue at position 211 (arginine in ZIKV, lysine in DENV2/JEV) as critical for the unwinding activity of ZIKV and JEV NS1, but dispensable for DENV2 NS1. These findings indicate that flavivirus NS1 represents a previously unrecognized non-canonical RNA helicase, suggesting that NS1 may have the capacity to participate in RNA remodeling processes.
-
7. Synergistic effect of combinational SHEN26 and PF07817883 in SARS-CoV-2 infection.
PMID:日期:2026-09-11该文献暂无摘要。
-
8. Update on BA.3.2 epidemiology: Evidence for co-circulation and preferential infection of children.
PMID:日期:2026-09-11该文献暂无摘要。
-
9. Epidemiological Characteristics and In-Hospital Burden of Infectious Mononucleosis Among Hospitalized Children in China, 2021-2023.
PMID:日期:2026-09-10This multicenter study described the epidemiological characteristics, recorded first-ranked secondary diagnoses, and in-hospital burden of pediatric infectious mononucleosis (IM) hospitalizations in China during 2021-2023. Data were obtained from the FUTURE database. We identified hospitalizations with IM as the principal discharge diagnosis from discharge-record front pages at 31 tertiary children's hospitals between January 1, 2021, and December 31, 2023, and analyzed demographic, geographic, temporal, diagnostic, length-of-stay (LOS), and expense data using descriptive statistics and multivariable regression. Among 15,239 IM hospitalizations, representing 0.42% of all hospitalizations, the male-to-female ratio was 1.34. Children aged 4-6 years comprised the largest group, followed by those aged 1-3 and 7-12 years; 70.32% were urban residents, and admissions peaked in August and September. After adjustment for age, sex, seven-category geographic area, and month, the proportion of IM hospitalizations among all hospitalizations was lower in 2023 than in 2021-2022 (adjusted rate ratio, 0.822; 95% CI, 0.784-0.861; P < 0.001). A first-ranked secondary diagnosis was recorded in 68.29% of cases; bronchitis/pneumonia was the most common category, followed by hepatic dysfunction. Median LOS was 7 days, and median hospitalization expense was CNY 5,563.07. Encephalitis was recorded in only 15 cases but had the longest descriptive LOS and highest descriptive expenses. These findings provide a large multicenter baseline for the epidemiological patterns and in-hospital burden of pediatric IM hospitalizations across participating tertiary children's hospitals in China and may inform future surveillance and resource planning.
-
10. A HiBiT-Tagged influenza A virus reporter system reveals cytokine-inhibitory micropeptide 53 as a modulator of viral infection and immunopathology.
PMID:日期:2026-09-05Influenza A virus (IAV) remains a major threat to human and animal health, highlighting the need for efficient approaches to identify host factors and antivirals. Reporter viruses are critical tools for these efforts, but incorporating large reporter genes often compromises viral fitness and genetic stability. Here, we developed a replication competent reporter IAV by fusing an 11-amino acid HiBiT tag into the nonstructural protein 1 (NS1) of the A/WSN/1933 (H1N1) backbone. The modified virus retained parental virion morphology, comparable replication kinetics, and in vivo tissue tropism, while enabling the highly sensitive, rapid, and quantitative detection of viral replication. Using this reporter virus, we established a robust high-throughput screening (HTS) platform with excellent assay quality and validated its capability to identify host regulators of IAV infection. Application of this platform to host-encoded micropeptides (miPEPs) led to the identification of cytokine-inhibitory micropeptide 53 (CIM53) as a novel regulator of IAV replication. Mechanistically, CIM53 promoted IAV replication by intrinsically suppressing antiviral innate immune responses. Furthermore, although CIM53 enhanced viral replication, its immunomodulatory activity contributed to reduced lung injury and improved survival when combined with Oseltamivir (OSV) treatment in infected mice. Our study establishes a highly practical screening platform for virological research and highlights CIM53 as a potential host-directed adjunct therapy for severe IAV infection.