首页期刊导航|中国病毒学
期刊信息/Journal information
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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    Persistent inflammation and neuronal loss in the mouse brain induced by a modified form of attenuated herpes simplex virus type Ⅰ

    Erlin WangXinwei HuangYunshuang YeShiqing Zou...
    108-118页
    查看更多>>摘要：Herpes simplex virus-1(HSV-1)is a widespread neurotropic virus that can reach the brain and cause a rare but acute herpes simplex encephalitis(HSE)with a high mortality rate.Most patients present with changes in neurological and behavioral status,and survivors suffer long-term neurological sequelae.To date,the patho-genesis leading to brain damage is still not well understood.HSV-1 induced encephalitis in the central nervous system(CNS)in animals are usually very diffuse and progressing rapidly,and mostly fatal,making the analysis difficult.Here,we established a mouse model of HSE via intracerebral inoculation of modified version of neural-attenuated strains of HSV-1(deletion of ICP34.5 and inserting a strong promoter into the latency-associated transcript region),in which the LMR-αΔpA strain initiated moderate productive infection,leading to strong host immune and inflammatory response characterized by persistent microglia activation.This viral replication activity and prolonged inflammatory response activated signaling pathways in neuronal damage,amyloidosis,Alzheimer's disease,and neurodegeneration,eventually leading to neuronal loss and behavioral changes char-acterized by hypokinesia.Our study reveals detailed pathogenic processes and persistent inflammatory responses in the CNS and provides a controlled,mild and non-lethal HSE model for studying long-term neuronal injury and increased risk of neurodegenerative diseases due to HSV-1 infection.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Taurolidine improved protection against highly pathogenetic avian influenza H5N1 virus lethal-infection in mouse model by regulating the NF-κB signaling pathway

    Chaoxiang LvYuanguo LiTiecheng WangQiqi Zhang...
    119-127页
    查看更多>>摘要：Taurolidine(TRD),a derivative of taurine,has anti-bacterial and anti-tumor effects by chemically reacting with cell-walls,endotoxins and exotoxins to inhibit the adhesion of microorganisms.However,its application in antiviral therapy is seldom reported.Here,we reported that TRD significantly inhibited the replication of influenza virus H5N1 in MDCK cells with the half-maximal inhibitory concentration(EC50)of 34.45 μg/mL.Furthermore,the drug inhibited the amplification of the cytokine storm effect and improved the survival rate of mice lethal challenged with H5N1(protection rate was 86％).Moreover,TRD attenuated virus-induced lung damage and reduced virus titers in mice lungs.Administration of TRD reduced the number of neutrophils and increased the number of lymphocytes in the blood of H5N1 virus-infected mice.Importantly,the drug regulated the NF-κB signaling pathway by inhibiting the separation of NF-κB and IκBa,thereby reducing the expression of inflammatory factors.In conclusion,our findings suggested that TRD could act as a potential anti-influenza drug candidate in further clinical studies.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Nonmuscle myosin ⅡA promotes the internalization of influenza A virus and regulates viral polymerase activity through interacting with nucleoprotein in human pulmonary cells

    Jian ChenJian LiuZhilu ChenDaobin Feng...
    128-141页
    查看更多>>摘要：Influenza A virus(IAV),responsible for seasonal epidemics and recurring pandemics,represents a global threat to public health.Given the risk of a potential IAV pandemic,it is increasingly important to better understand virus-host interactions and develop new anti-viral strategies.Here,we reported nonmuscle myosin ⅡA(MYH9)-mediated regulation of IAV infection.MYH9 depletion caused a profound inhibition of IAV infection by reducing viral attachment and internalization in human lung epithelial cells.Surprisingly,overexpression of MYH9 also led to a significant reduction in viral productive infection.Interestingly,overexpression of MYH9 retained viral attachment,internalization,or uncoating,but suppressed the viral ribonucleoprotein(vRNP)activity in a mini-genome system.Further analyses found that excess MYH9 might interrupt the formation of vRNP by interacting with the viral nucleoprotein(NP)and result in the reduction of the completed vRNP in the nucleus,thereby inhibiting subsequent viral RNA transcription and replication.Together,we discovered that MYH9 can interact with IAV NP protein and engage in the regulation of vRNP complexes,thereby involving viral replication.These findings enlighten new mechanistic insights into the complicated interface of host-IAV interactions,ultimately making it an attractive target for the generation of antiviral drugs.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    GCRV NS38 counteracts SVCV proliferation by intracellular antagonization during co-infection

    Zhuo-Cong LiLong-Feng LuCan ZhangXue-Li Wang...
    142-156页
    查看更多>>摘要：Viral co-infection has been found in animals;however,the mechanisms of co-infection are unclear.The abun-dance and diversity of viruses in water make fish highly susceptible to co-infection.Here,we reported a co-infection in fish,which resulted in reduced host lethality and illustrated the intracellular molecular mechanism of viral co-infection.The spring viremia of carp virus(SVCV)is a highly lethal virus that infects Cyprinidae,such as zebrafish.The mortality of SVCV infection was significantly reduced when co-infected with the grass carp reovirus(GCRV).The severity of tissue damage and viral proliferation of SVCV was also reduced in co-infection with GCRV.The transcriptome bioinformatics analysis demonstrated that the effect on the host transcripts in response to SVCV infection was significantly reduced in co-infection.After excluding the extracellular interactions of these two viruses,the intracellular mechanisms were studied.We found that the GCRV NS38 remarkably decreased SVCV infection and viral proliferation.The interaction between GCRV NS38 and SVCV nucleoprotein(N)and phosphoprotein(P)proteins was identified,and NS38 downregulated both N and P proteins.Further analysis demonstrated that the N protein was degraded by NS38 indispensable of the autophagy receptor,sequestosome 1(p62).Meanwhile,K63-linked ubiquitination of the P protein was reduced by NS38,leading to ubiquitinated degradation of the P protein.These results reveal that the intracellular viral protein interactions are a crucial mechanism of co-infection and influence the host pathology and expand our understanding in intra-cellular viral interactions co-infection.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Emergence of H5N8 avian influenza virus in domestic geese in a wild bird habitat,Yishui Lake,north central China

    Cheng ZhangZhong-Yi WangHuan CuiLi-Gong Chen...
    157-161页
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Immunization of mice with vaccinia virus Tiantan strain yields antibodies cross-reactive with protective antigens of monkeypox virus

    Lei YangYingshan ChenSha LiYuan Zhou...
    162-164页
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Development of rapid nucleic acid assays based on the recombinant polymerase amplification for monkeypox virus

    Yuchang LiYanhong GaoYing TangJing Li...
    165-170页
      原文链接:
    • NETL
    • NSTL
    • 万方数据