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中国病毒学
中国病毒学

陈新文

双月刊

1674-0769

bjb@wh.iov.cn

027-87199157

430071

武汉武昌区小洪山中区44号

中国病毒学/Journal Virologica SinicaCSCD北大核心CSTPCDSCI
查看更多>>本刊由中国科学院武汉病毒研究所、中国微生物学会共同主办、科学出版社出版的学术性双月刊，创刊于1986年，原名为《病毒学杂志》(Virologica　Sinica)，季刊。1991年更名为《中国病毒学》，外文刊名不变，2003年改为双月刊，自创刊以来，发表病毒学研究论文1000多篇，发表论文基金率为65%以上。曾三次荣获湖北省优秀期刊奖，被评为中国生物学核心期刊、基础医学类核心期刊和中国科学引文数据库核心期刊。长期被BA（生物学文摘）、CA（化学文摘）和中国生物学文摘、医学文摘、农业学文摘等国内外20余种文摘及检索刊物收录，为国家科技部信息所“万方数据（ChinaInfo）系统”、清华大学“中国学术期刊光盘版”和“中国期刊网”的期刊源。是CSCI　(中国科学引文索引)、中国生物学和医学期刊的核心期刊。影响因子为0.553　(2003年统计数据)
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    Host cell restriction factors of equine infectious anemia virus

    Xue-Feng WangXiangmin ZhangWeiwei MaJiwei Li...
    485-496页
    查看更多>>摘要：Equine infectious anemia virus(EIAV)is a member of the lentivirus genus in the Retroviridae family and is considered an animal model for HIV/AIDS research.An attenuated EIAV vaccine,which was successfully developed in the 1970s by classical serial passage techniques,is the first and only lentivirus vaccine that has been widely used to date.Restriction factors are cellular proteins that provide an early line of defense against viral replication and spread by interfering with various critical steps in the viral replication cycle.However,viruses have evolved specific mechanisms to overcome these host barriers through adaptation.The battle between the viruses and restriction factors is actually a natural part of the viral replication process,which has been well studied in human immunodeficiency virus type 1(HIV-1).EIAV has the simplest genome composition of all lenti viruses,making it an intriguing subject for understanding how the virus employs its limited viral proteins to overcome restriction factors.In this review,we summarize the current literature on the interactions between equine restriction factors and EIAV.The features of equine restriction factors and the mechanisms by which the EIAV counteract the restriction suggest that lentiviruses employ diverse strategies to counteract innate immune restrictions.In addition,we present our insights on whether restriction factors induce alterations in the phenotype of the attenuated EIAV vaccine.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Elucidating cellular interactome of chikungunya virus identifies host dependency factors

    Peiqi YinXia JianYihan LiuYuwen Liu...
    497-507页
    查看更多>>摘要：Chikungunya virus(CHIKV)is a re-emerging mosquito-transmitted RNA virus causing joint and muscle pain.To better understand how CHIKV rewires the host cell and usurps host cell functions,we generated a systematic CHIKV-human protein-protein interaction map and revealed several novel connections that will inform further mechanistic studies.One of these novel interactions,between the viral protein E1 and STIP1 homology and U-box containing protein 1(STUB1),was found to mediate ubiquitination of E1 and degrade E1 through the proteasome.Capsid associated with G3BP1,G3BP2 and AAA+ATPase valosin-containing protein(VCP).Furthermore,VCP inhibitors blocked CHIKV infection,suggesting VCP could serve as a therapeutic target.Further work is required to fully understand the functional consequences of these interactions.Given that CHIKV proteins are conserved across alphaviruses,many virus-host protein-protein interactions identified in this study might also exist in other alphaviruses.Construction of interactome of CHIKV provides the basis for further studying the function of alphavirus biology.
      原文链接:
    • NETL
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    • 万方数据

    Integrated interactome and transcriptome analysis reveals key host factors critical for SARS-CoV-2 infection

    Jie ShengLili LiXueying LvMeiling Gao...
    508-519页
    查看更多>>摘要：The coronavirus disease 2019(COVID-19)pandemic,caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has seriously threatened global public health and caused huge economic losses.Omics studies of SARS-CoV-2 can help understand the interaction between the virus and host,thereby providing a new perspective in guiding the intervention and treatment of the SARS-CoV-2 infection.Since large amount of SARS-CoV-2 omics data have been accumulated in public databases,this study aimed to identify key host factors involved in SARS-CoV-2 infection through systematic integration of transcriptome and interactome data.By manually curating published studies,we obtained a comprehensive SARS-CoV-2-human protein-protein interactions(PPIs)network,comprising 3591 human proteins interacting with 31 SARS-CoV-2 viral proteins.Using the RobustRankAg-gregation method,we identified 123 multiple cell line common genes(CLCGs),of which 115 up-regulated CLCGs showed host enhanced innate immunity and chemotactic response signatures.Combined with network analysis,co-expression and functional enrichment analysis,we discovered four key host factors involved in SARS-CoV-2 infection:IFITM1,SERPINE1,DDX60,and TNFAIP2.Furthermore,SERPINE1 was found to facilitate SARS-CoV-2 replication,and can alleviate the endoplasmic reticulum(ER)stress induced by ORF8 protein through interaction with ORF8.Our findings highlight the importance of systematic integration analysis in understanding SARS-CoV-2-human interactions and provide valuable insights for future research on potential therapeutic targets against SARS-CoV-2 infection.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    SARS-CoV-2 Nsp8 induces mitophagy by damaging mitochondria

    Shan ZongYan WuWeiling LiQiang You...
    520-530页
    查看更多>>摘要：Autophagy plays an important role in the interaction between viruses and host cells.SARS-CoV-2 infection can disrupt the autophagy process in target cells.However,the precise molecular mechanism is still unknown.In this study,we discovered that the Nsp8 of SARS-CoV-2 could cause an increasing accumulation of autophagosomes by preventing the fusion of autophagosomes and lysosomes.From further investigation,we found that Nsp8 was present on mitochondria and can damage mitochondria to initiate mitophagy.The results of experiments with immunofluorescence revealed that Nsp8 induced incomplete mitophagy.Moreover,both domains of Nsp8 orchestrated their function during Nsp8-induced mitophagy,in which the N-terminal domain colocalized with mitochondria and the C-terminal domain induced auto/mitophagy.This novel finding expands our understanding of the function of Nsp8 in promoting mitochondrial damage and inducing incomplete mitophagy,which helps us to understand the etiology of COVID-19 as well as open up new pathways for creating SARS-CoV-2 treatment methods.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Unusual substructure conformations observed in crystal structures of a dicistrovirus RNA-dependent RNA polymerase suggest contribution of the N-terminal extension in proper folding

    Xiang FangGuoliang LuYanchun DengSa Yang...
    531-540页
    查看更多>>摘要：The Dicistroviridae is a virus family that includes many insect pathogens.These viruses contain a positive-sense RNA genome that is replicated by the virally encoded RNA-dependent RNA polymerase(RdRP)also named 3Dpol.Compared with the Picornaviridae RdRPs such as poliovirus(PV)3Dpol,the Dicistroviridae representative Israeli acute paralysis virus(IAPV)3Dpol has an additional N-terminal extension(NE)region that is about 40-res-idue in length.To date,both the structure and catalytic mechanism of the Dicistroviridae RdRP have remain elusive.Here we reported crystal structures of two truncated forms of IAPV 3Dpol,namely Δ85 and Δ40,both missing the NE region,and the 3Dpol protein in these structures exhibited three conformational states.The palm and thumb domains of these IAPV 3Dpol structures are largely consistent with those of the PV 3Dpol structures.However,in all structures,the RdRP fingers domain is partially disordered,while different conformations of RdRP substructures and interactions between them are also present.In particular,a large-scale conformational change occurred in the motif B-middle finger region in one protein chain of the Δ40 structure,while a previously documented alternative conformation of motif A was observed in all IAPV structures.These experimental data on one hand show intrinsic conformational variances of RdRP substructures,and on the other hand suggest possible contribution of the NE region in proper RdRP folding in IAPV.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Development of PREDAC-H1pdm to model the antigenic evolution of influenza A/(H1N1)pdm09 viruses

    Mi LiuJingze LiuWenjun SongYousong Peng...
    541-548页
    查看更多>>摘要：The Influenza A(H1N1)pdm09 virus caused a global pandemic in 2009 and has circulated seasonally ever since.As the continual genetic evolution of hemagglutinin in this virus leads to antigenic drift,rapid identification of antigenic variants and characterization of the antigenic evolution are needed.In this study,we developed PREDAC-H1pdm,a model to predict antigenic relationships between H1N1pdm viruses and identify antigenic clusters for post-2009 pandemic H1N1 strains.Our model performed well in predicting antigenic variants,which was helpful in influenza surveillance.By mapping the antigenic clusters for H1N1pdm,we found that sub-stitutions on the Sa epitope were common for H1N1pdm,whereas for the former seasonal H1N1,substitutions on the Sb epitope were more common in antigenic evolution.Additionally,the localized epidemic pattern of H1N1pdm was more obvious than that of the former seasonal H1N1,which could make vaccine recommendation more sophisticated.Overall,the antigenic relationship prediction model we developed provides a rapid deter-mination method for identifying antigenic variants,and the further analysis of evolutionary and epidemic characteristics can facilitate vaccine recommendations and influenza surveillance for H1N1pdm.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Construction of coxsackievirus B5 viruses with luciferase reporters and their applications in vitro and in vivo

    Shangrui GuoMeng XunTingting FanXinyu Li...
    549-558页
    查看更多>>摘要：Coxsackievirus belongs to the Picornaviridae family and is one of the major pathogens that cause hand,foot and mouth disease(HFMD)in infants and children with potential serious complications and even deaths.The path-ogenesis of this virus is not fully elucidated and no vaccine or antiviral drug has been approved.In this study,a full-length infectious cDNA clone of coxsackievirus B5 virus was assembled and the recombinant virus displayed similar growth kinetics and ability to cause cytopathic effects as the parental virus.Luciferase reporter was then incorporated to generate both full-length and subgenomic replicon(SGR)reporter viruses.The full-length reporter virus is suitable for high-throughput antiviral screening,while the SGR is a useful tool to study viral-host in-teractions.More importantly,the full-length reporter virus has also been shown to infect the suckling mouse model and the reporter gene could be detected using an in vivo imaging system,thus providing a powerful tool to track viruses in vivo.In summary,we have generated coxsackievirus B5 reporter viruses and provided unique tools for studying virus-host interactions in vitro and in vivo as well as for high-throughput screenings(HTS)to identify novel antivirals.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    PA-E18G substitution in influenza A virus confers resistance to ZX-7101,a cap-dependent endonuclease inhibitor

    Dan LuoQing YeRui-Ting LiHang-Yu Zhou...
    559-567页
    查看更多>>摘要：Cap-dependent endonuclease(CEN)in the polymerase acidic protein(PA)of influenza A virus(IAV)represents a promising drug target due to its critical role in viral gene transcription.The CEN inhibitor,baloxavir marboxil(BXM),was approved in Japan and the US in 2018 and several other countries subsequently.Along with the clinical use of BXM,the emergence and spread of IAV variants with reduced susceptibility to BXM have aroused serious concern.Herein,we comprehensively characterized the in vitro and in vivo antiviral activities of ZX-7101 A,an analogue of BXM.The active form of prodrug ZX-7101 showed broad-spectrum antiviral potency against various IAV subtypes,including pH1N1,H3N2,H7N9 and H9N2,in MDCK cells,and the 50％effective con-centration(EC50)was calculated to nanomole level and comparable to that of baloxavir acid(BXA),the active form of BXM.Furthermore,in vivo assays showed that administration of ZX-7101A conferred significant pro-tection against lethal pH1N1 challenge in mice,with reduced viral RNA loads and alleviated pulmonary damage.Importantly,serial passaging of H1N1 virus in MDCK cells under selection pressure of ZX-7101 led to a resistant variant at the 15th passage.Reverse genetic and sequencing analysis demonstrated that a single E18G substitution in the PA subunit contributed to the reduced susceptibility to both ZX-7101 and BXA.Taken together,our results not only characterized a new CEN inhibitor of IAV but also identified a novel amino acid substitution responsible for CEN inhibitor resistance,which provides critical clues for future drug development and drug resistance surveillance.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    STING strengthens host anti-hantaviral immunity through an interferon-independent pathway

    Kerong WangJian ZhangYongheng YangYue Si...
    568-584页
    查看更多>>摘要：Hantaan virus(HTNV),the prototype virus of hantavirus,could escape innate immunity by restraining type Ⅰ interferon(IFN)responses.It is largely unknown whether there existed other efficient anti-hantaviral tactics in host cells.Here,we demonstrate that the stimulator of interferon genes(STING)strengthens the host IFN-independent anti-hantaviral immunity.HTNV infection activates RIG-I through IRE1-XBP 1-mediated ER stress,which further facilitates the subcellular translocation and activation of STING.During this process,STING triggers cellular autophagy by interacting with Rab7A,thus restricting viral replication.To note,the anti-hantaviral effects of STING are independent of canonical IFN signaling.Additionally,neither application of the pharmacological antagonist nor the agonist targeting STING could improve the outcomes of nude mice post HTNV challenge in vivo.However,the administration of plasmids exogenously expressing the mutant C-terminal tail(ACTT)STING,which would not trigger the type Ⅰ IFN responses,protected the nude mice from lethal HTNV infection.In summary,our research revealed a novel antiviral pathway through the RIG-I-STING-autophagy pathway,which offered novel therapeutic strategies against hantavirus infection.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    A high throughput antiviral screening platform for alphaviruses based on Semliki Forest virus expressing eGFP reporter gene

    Yu-Jia ShiJia-Qi LiHong-Qing ZhangCheng-Lin Deng...
    585-594页
    查看更多>>摘要：Alphaviruses,which contain a variety of mosquito-borne pathogens,are important pathogens of emerging/re-emerging infectious diseases and potential biological weapons.Currently,no specific antiviral drugs are avail-able for the treatment of alphaviruses infection.For most highly pathogenic alphaviruses are classified as risk group-3 agents,the requirement of biosafety level 3(BSL-3)facilities limits the live virus-based antiviral study.To facilitate the antiviral development of alphaviruses,we developed a high throughput screening(HTS)platform based on a recombinant Semliki Forest virus(SFV)which can be manipulated in BSL-2 laboratory.Using the reverse genetics approach,the recombinant SFV and SFV reporter virus expressing eGFP(SFV-eGFP)were suc-cessfully rescued.The SFV-eGFP reporter virus exhibited robust eGFP expression and remained relatively stable after four passages in BHK-21 cells.Using a broad-spectrum alphavirus inhibitor ribavirin,we demonstrated that the SFV-eGFP can be used as an effective tool for antiviral study.The SFV-eGFP reporter virus-based HTS assay in a 96-well format was then established and optimized with a robust Z'score.A section of reference compounds that inhibit highly pathogenic alphaviruses were used to validate that the SFV-eGFP reporter virus-based HTS assay enables rapid screening of potent broad-spectrum inhibitors of alphaviruses.This assay provides a safe and convenient platform for antiviral study of alphaviruses.
      原文链接:
    • NETL
    • NSTL
    • 万方数据