Virologica Sinica最新文献

{"title":"Mice with type I interferon signaling deficiency are prone to epilepsy upon HSV-1 infection","authors":"Wei Yang ,&nbsp;Chong-Yang Tang ,&nbsp;Dong-Ying Fan ,&nbsp;Yi-Song Wang ,&nbsp;Pei-Gang Wang ,&nbsp;Jing An ,&nbsp;Guo-Ming Luan","doi":"10.1016/j.virs.2024.01.002","DOIUrl":"10.1016/j.virs.2024.01.002","url":null,"abstract":"<div><p>Viral encephalitis continues to be a significant public health concern. In our previous study, we discovered a lower expression of antiviral factors, such as IFN-β, STING and IFI16, in the brain tissues of patients with Rasmussen's encephalitis (RE), a rare chronic neurological disorder often occurred in children, characterized by unihemispheric brain atrophy. Furthermore, a higher cumulative viral score of human herpes viruses (HHVs) was also found to have a significant positive correlation with the unihemispheric atrophy in RE. Type I IFNs (IFN-I) signaling is essential for innate anti-infection response by binding to IFN-α/β receptor (IFNAR). In this study, we infected WT mice and IFNAR-deficient A6 mice with herpes simplex virus 1 (HSV-1) via periocular injection to investigate the relationship between IFN-I signaling and HHVs-induced brain lesions. While all mice exhibited typical viral encephalitis lesions in their brains, HSV-induced epilepsy was only observed in A6 mice. The gene expression matrix, functional enrichment analysis and protein-protein interaction network revealed four gene models that were positively related with HSV-induced epilepsy. Additionally, ten key genes with the highest scores were identified. Taken together, these findings indicate that intact IFN-I signaling can effectively limit HHVs induced neural symptoms and brain lesions, thereby confirming the positive correlation between IFN-I signaling repression and brain atrophy in RE and other HHVs encephalitis.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X24000026/pdfft?md5=f41a52ba029cf8c31729482d38daa75f&pid=1-s2.0-S1995820X24000026-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139467091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “3Cpro of FMDV inhibits type II interferon-stimulated JAK-STAT signaling pathway by blocking STAT1 nuclear translocation” [Virol Sin 38 (2023) 387–397]","authors":"Xiangju Wu ,&nbsp;Lei Chen ,&nbsp;Chao Sui ,&nbsp;Yue Hu ,&nbsp;Dandan Jiang ,&nbsp;Fan Yang ,&nbsp;Laura C. Miller ,&nbsp;Juntong Li ,&nbsp;Xiaoyan Cong ,&nbsp;Nataliia Hrabchenko ,&nbsp;Changhee Lee ,&nbsp;Yijun Du ,&nbsp;Jing Qi","doi":"10.1016/j.virs.2023.12.007","DOIUrl":"10.1016/j.virs.2023.12.007","url":null,"abstract":"","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X23001608/pdfft?md5=de45e282ae149268dace91beb2e1cdda&pid=1-s2.0-S1995820X23001608-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139571469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interconnection of cellular autophagy and endosomal vesicle trafficking and its role in hepatitis B virus replication and release","authors":"Jia Li ,&nbsp;Yong Lin ,&nbsp;Xueyu Wang ,&nbsp;Mengji Lu","doi":"10.1016/j.virs.2024.01.001","DOIUrl":"10.1016/j.virs.2024.01.001","url":null,"abstract":"<div><p>Hepatitis B virus (HBV) produces and releases various particle types, including complete virions, subviral particles with envelope proteins, and naked capsids. Recent studies demonstrate that HBV exploits distinct intracellular membrane trafficking pathways, including the endosomal vesicle trafficking and autophagy pathway, to assemble and release viral and subviral particles. Herein, we summarize the findings about the distinct roles of autophagy and endosomal membrane trafficking and the interaction of both pathways in HBV replication, assembly, and release.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X24000014/pdfft?md5=c73d68376191040718efb2fbc8f412c6&pid=1-s2.0-S1995820X24000014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139425563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis contributes to JEV-induced neuronal damage and neuroinflammation","authors":"Wenjing Zhu ,&nbsp;Qi Li ,&nbsp;Yong Yin ,&nbsp;Huanchun Chen ,&nbsp;Youhui Si ,&nbsp;Bibo Zhu ,&nbsp;Shengbo Cao ,&nbsp;Zikai Zhao ,&nbsp;Jing Ye","doi":"10.1016/j.virs.2023.12.004","DOIUrl":"10.1016/j.virs.2023.12.004","url":null,"abstract":"<div><p>Ferroptosis is a newly discovered prototype of programmed cell death (PCD) driven by iron-dependent phospholipid peroxidation ​accumulation, and it has been linked to numerous organ injuries and degenerative pathologies. Although studies have shown that a variety of cell death processes contribute to JEV-induced neuroinflammation and neuronal injury, there is currently limited research on the specific involvement of ferroptosis. In this study, we explored the neuronal ferroptosis induced by JEV infection <em>in vitro</em> and <em>in vivo</em>. Our results indicated that JEV infection induces neuronal ferroptosis through inhibiting the function of the antioxidant system mediated by glutathione (GSH)/glutathione peroxidase 4 (GPX4), as well as by promoting lipid peroxidation mediated by yes-associated protein 1 (YAP1)/long-chain acyl-CoA synthetase 4 (ACSL4). Further analyses revealed that JEV E and prM proteins function as agonists, inducing ferroptosis. Moreover, we found that treatment with a ferroptosis inhibitor in JEV-infected mice reduces the viral titers and inflammation in the mouse brains, ultimately improving the survival rate of infected mice. In conclusion, our study unveils a critical role of ferroptosis in the pathogenesis of JEV, providing new ideas for the prevention and treatment of viral encephalitis.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X23001566/pdfft?md5=e515cb7d1dc167809611203bdd188cd5&pid=1-s2.0-S1995820X23001566-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138686805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Issue Cover","authors":"","doi":"10.1016/S1995-820X(24)00012-9","DOIUrl":"https://doi.org/10.1016/S1995-820X(24)00012-9","url":null,"abstract":"","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X24000129/pdfft?md5=e16f206ee72badb78c48142f46b6c92b&pid=1-s2.0-S1995820X24000129-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139731869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA barcode segments for SARS-CoV-2 identification from HCoVs and SARSr-CoV-2 lineages","authors":"Changqiao You ,&nbsp;Shuai Jiang ,&nbsp;Yunyun Ding ,&nbsp;Shunxing Ye ,&nbsp;Xiaoxiao Zou ,&nbsp;Hongming Zhang ,&nbsp;Zeqi Li ,&nbsp;Fenglin Chen ,&nbsp;Yongliang Li ,&nbsp;Xingyi Ge ,&nbsp;Xinhong Guo","doi":"10.1016/j.virs.2024.01.006","DOIUrl":"10.1016/j.virs.2024.01.006","url":null,"abstract":"<div><p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen responsible for coronavirus disease 2019 (COVID-19), continues to evolve, giving rise to more variants and global reinfections. Previous research has demonstrated that barcode segments can effectively and cost-efficiently identify specific species within closely related populations. In this study, we designed and tested RNA barcode segments based on genetic evolutionary relationships to facilitate the efficient and accurate identification of SARS-CoV-2 from extensive virus samples, including human coronaviruses (HCoVs) and SARSr-CoV-2 lineages. Nucleotide sequences sourced from NCBI and GISAID were meticulously selected and curated to construct training sets, encompassing 1733 complete genome sequences of HCoVs and SARSr-CoV-2 lineages. Through genetic-level species testing, we validated the accuracy and reliability of the barcode segments for identifying SARS-CoV-2. Subsequently, 75 main and subordinate species-specific barcode segments for SARS-CoV-2, located in <em>ORF1ab</em>, <em>S</em>, <em>E</em>, <em>ORF7a</em>, and <em>N</em> coding sequences, were intercepted and screened based on single-nucleotide polymorphism sites and weighted scores. Post-testing, these segments exhibited high recall rates (nearly 100%), specificity (almost 30% at the nucleotide level), and precision (100%) performance on identification. They were eventually visualized using one and two-dimensional combined barcodes and deposited in an online database (<span>http://virusbarcodedatabase.top/</span><svg><path></path></svg>). The successful integration of barcoding technology in SARS-CoV-2 identification provides valuable insights for future studies involving complete genome sequence polymorphism analysis. Moreover, this cost-effective and efficient identification approach also provides valuable reference for future research endeavors related to virus surveillance.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X24000063/pdfft?md5=d17814d2aee23bb4d075d608e8b938aa&pid=1-s2.0-S1995820X24000063-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139508329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutual antagonism of mouse-adaptation mutations in HA and PA proteins on H9N2 virus replication","authors":"Liping Ma ,&nbsp;Huabin Zheng ,&nbsp;Xianliang Ke ,&nbsp;Rui Gui ,&nbsp;Zhongzi Yao ,&nbsp;Jiasong Xiong ,&nbsp;Quanjiao Chen","doi":"10.1016/j.virs.2023.11.004","DOIUrl":"10.1016/j.virs.2023.11.004","url":null,"abstract":"<div><p>Avian H9N2 viruses have wide host range among the influenza A viruses. However, knowledge of H9N2 mammalian adaptation is limited. To explore the molecular basis of the adaptation to mammals, we performed serial lung passaging of the H9N2 strain A/chicken/Hunan/8.27 YYGK3W3-OC/2018 (3W3) in mice and identified six mutations in the hemagglutinin (HA) and polymerase acidic (PA) proteins. Mutations L226Q, T511I, and A528V of HA were responsible for enhanced pathogenicity and viral replication in mice; notably, HA-L226Q was the key determinant. Mutations T97I, I545V, and S594G of PA contributed to enhanced polymerase activity in mammalian cells and increased viral replication levels <em>in vitro</em> and <em>in vivo</em>. PA-T97I increased viral polymerase activity by accelerating the viral polymerase complex assembly. Our findings revealed that the viral replication was affected by the presence of PA-97I and/or PA-545V in combination with a triple-point HA mutation. Furthermore, the double- and triple-point PA mutations demonstrated antagonistic effect on viral replication when combined with HA-226Q. Notably, any combination of PA mutations, along with double-point HA mutations, resulted in antagonistic effect on viral replication. We also observed antagonism in viral replication between PA-545V and PA-97I, as well as between HA-528V and PA-545V. Our findings demonstrated that several antagonistic mutations in HA and PA proteins affect viral replication, which may contribute to the H9N2 virus adaptation to mice and mammalian cells. These findings can potentially contribute to the monitoring of H9N2 field strains for assessing their potential risk in mammals.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X23001360/pdfft?md5=5d0ce94edca65548346ad7cf839221fe&pid=1-s2.0-S1995820X23001360-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134649943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naturally occurring PAE206K point mutation in 2009 H1N1 pandemic influenza viruses impairs viral replication at high temperatures","authors":"Mengmeng Cao ,&nbsp;Qiannan Jia ,&nbsp;Jinghua Li ,&nbsp;Lili Zhao ,&nbsp;Li zhu ,&nbsp;Yufan Zhang ,&nbsp;Shan Li ,&nbsp;Tao Deng","doi":"10.1016/j.virs.2023.11.005","DOIUrl":"10.1016/j.virs.2023.11.005","url":null,"abstract":"<div><p>The emergence of influenza virus A pandemic H1N1 in April 2009 marked the first pandemic of the 21st century. In this study, we observed significant differences in the polymerase activities of two clinical 2009 H1N1 influenza A virus isolates from Chinese and Japanese patients. Sequence comparison of the three main protein subunits (PB2, PB1, and PA) of the viral RNA-dependent RNA polymerase complex and subsequent mutational analysis revealed that a single amino acid substitution (E206K) was responsible for the observed impaired replication phenotype. Further <em>in vitro</em> experiments showed that presence of PA^E206K decreased the replication of influenza A/WSN/33 virus in mammalian cells and a reduction in the virus’s pathogenicity <em>in vivo</em>. Mechanistic studies revealed that PA^E206K is a temperature-sensitive mutant associated with the inability to transport PB1–PA complex to the nucleus at high temperature (39.5 ​°C). Hence, this naturally occurring variant in the PA protein represents an ideal candidate mutation for the development of live attenuated influenza vaccines.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X23001372/pdfft?md5=1425bc5ea50e0aec0f8c786c33294580&pid=1-s2.0-S1995820X23001372-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138048062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ancient dormant virus remnant ERVW-1 drives ferroptosis via degradation of GPX4 and SLC3A2 in schizophrenia","authors":"Dongyan Zhang ,&nbsp;Xiulin Wu ,&nbsp;Xing Xue ,&nbsp;Wenshi Li ,&nbsp;Ping Zhou ,&nbsp;Zhao Lv ,&nbsp;Kexin Zhao ,&nbsp;Fan Zhu","doi":"10.1016/j.virs.2023.09.001","DOIUrl":"10.1016/j.virs.2023.09.001","url":null,"abstract":"<div><p>Human endogenous retroviruses (HERVs) are remnants of retroviral infections in human germline cells from millions of years ago. Among these, ERVW-1 (also known as HERV-W-ENV, ERVWE1, or ENVW) encodes the envelope protein of the HERV-W family, which contributes to the pathophysiology of schizophrenia. Additionally, neuropathological studies have revealed cell death and disruption of iron homeostasis in the brains of individuals with schizophrenia. Here, our bioinformatics analysis showed that differentially expressed genes in the human prefrontal cortex RNA microarray dataset (GSE53987) were mainly related to ferroptosis and its associated pathways. Clinical data demonstrated significantly lower expression levels of ferroptosis-related genes, particularly Glutathione peroxidase 4 (GPX4) and solute carrier family 3 member 2 (SLC3A2), in schizophrenia patients compared to normal controls. Further in-depth analyses revealed a significant negative correlation between ERVW-1 expression and the levels of GPX4/SLC3A2 in schizophrenia. Studies indicated that ERVW-1 increased iron levels, malondialdehyde (MDA), and transferrin receptor protein 1 (TFR1) expression while decreasing glutathione (GSH) levels and triggering the loss of mitochondrial membrane potential, suggesting that ERVW-1 can induce ferroptosis. Ongoing research has shown that ERVW-1 reduced the expression of GPX4 and SLC3A2 by inhibiting their promoter activities. Moreover, Ferrostatin-1 (Fer-1), the ferroptosis inhibitor, reversed the iron accumulation and mitochondrial membrane potential loss, as well as restored the expressions of ferroptosis markers GSH, MDA, and TFR1 induced by ERVW-1. In conclusion, ERVW-1 could promote ferroptosis by downregulating the expression of GPX4 and SLC3A2, revealing a novel mechanism by which ERVW-1 contributes to neuronal cell death in schizophrenia.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X23001098/pdfft?md5=702ada9c8d00b7fc431cfd7923ae9a4e&pid=1-s2.0-S1995820X23001098-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10569968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsp90 β is critical for the infection of severe fever with thrombocytopenia syndrome virus","authors":"Bo Wang ,&nbsp;Leike Zhang ,&nbsp;Fei Deng ,&nbsp;Zhihong Hu ,&nbsp;Manli Wang ,&nbsp;Jia Liu","doi":"10.1016/j.virs.2023.11.008","DOIUrl":"10.1016/j.virs.2023.11.008","url":null,"abstract":"<div><p>Severe fever with thrombocytopenia syndrome (SFTS) caused by the SFTS virus (SFTSV) is an emerging disease in East Asia with a fatality rate of up to 30%. However, the viral-host interaction of SFTSV remains largely unknown. The heat-shock protein 90 (Hsp90) family consists of highly conserved chaperones that fold and remodel proteins and has a broad impact on the infection of many viruses. Here, we showed that Hsp90 is an important host factor involved in SFTSV infection. Hsp90 inhibitors significantly reduced SFTSV replication, viral protein expression, and the formation of inclusion bodies consisting of nonstructural proteins (NSs). Among viral proteins, NSs appeared to be the most reduced when Hsp90 inhibitors were used, and further analysis showed that their translation was affected. Co-immunoprecipitation of NSs with four isomers of Hsp90 showed that Hsp90 β specifically interacted with them. Knockdown of Hsp90 β expression also inhibited replication of SFTSV. These results suggest that Hsp90 β plays a critical role during SFTSV infection and could be a potential target for the development of drugs against SFTS.</p></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":null,"pages":null},"PeriodicalIF":5.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1995820X23001402/pdfft?md5=1c7d6d6565b09c12e2985d25783ccb1b&pid=1-s2.0-S1995820X23001402-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138441267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}