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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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    Diversity and independent evolutionary profiling of rodent-borne viruses in Hainan,a tropical island of China

    Youyou LiChuanning TangYun ZhangZihan Li...
    651-662页
    查看更多>>摘要：The risk of emerging infectious diseases(EID)is increasing globally.More than 60％of EIDs worldwide are caused by animal-borne pathogens.This study aimed to characterize the virome,analyze the phylogenetic evolution,and determine the diversity of rodent-borne viruses in Hainan Province,China.We collected 682 anal and throat samples from rodents,combined them into 28 pools according to their species and location,and processed them for next-generation sequencing and bioinformatics analysis.The diverse viral contigs closely related to mammals were assigned to 22 viral families.Molecular clues of the important rodent-borne viruses were further identified by polymerase chain reaction for phylogenetic analysis and annotation of genetic characteristics such as arena-virus,coronavirus,astrovirus,pestivirus,parvovirus,and papillomavirus.We identified pestivirus and bocavirus in Leopoldoms edwardsi from Huangjinjiaoling,and bocavirus in Rattus andamanensis from the national nature reserves of Bangxi with low amino acid identity to known pathogens are proposed as the novel species,and their rodent hosts have not been previously reported to carry these viruses.These results expand our knowledge of viral classification and host range and suggest that there are highly diverse,undiscovered viruses that have evolved independently in their unique wildlife hosts in inaccessible areas.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Epizootiological surveillance of porcine circoviruses in free-ranging wild boars in China

    Wenjie GongHaiying DuTong WangHeting Sun...
    663-670页
    查看更多>>摘要：Four species of porcine circoviruses(PCV1-4)have been reported to circulate in Chinese domestic pigs,while the epizootiology of these viruses in free-ranging wild boars in China remains unknown.In this study,tissue and serum samples collected from diseased or apparently healthy wild boars between 2018 and 2020 in 19 regions of China were tested for the prevalence of PCV1-4 infections.Positive rates of PCV1,PCV2,and PCV3 DNA in the tissue samples of Chinese wild boars were 1.6％(4/247),58.3％(144/247),and 10.9％(27/247)respectively,with none positive for PCV4.Sequence analysis of viral genome showed that the four PCV1 strains distributed in Hunan and Inner Mongolia shared 97.5％-99.6％sequence identity with global distributed reference strains.Comparison of the ORF2 gene sequences showed that 80 PCV2 strains widely distributed in 18 regions shared 79.5％-100％sequence identity with reference strains from domestic pigs and wild boars,and were grouped into PCV2a(7),PCV2b(31)and PCV2d(42).For PCV3,17 sequenced strains shared 97.2％-100％nucleotide identity at the genomic level and could be divided into PCV3a(3),PCV3b(2)and PCV3c(12)based on the phylogeny of ORF2 gene sequences.Serological data revealed antibody positive rates against PCV1 and PCV2 of 11.4％(19/167)and 53.9％(90/167)respectively.The data obtained in this study improved our understanding about the epidemiological situations of PCVs infection in free-ranging wild boars in China and will be valuable for the prevention and control of diseases caused by PCVs infection.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Changing predominance of norovirus strains in children with acute gastroenteritis in Shanghai,2018-2021

    Lijuan LuYuanyun AoRan JiaHuaqing Zhong...
    671-679页
    查看更多>>摘要：Norovirus(NoV)is a major pathogen that causes acute gastroenteritis(AGE)in people of all ages,especially in children.In this study,we investigated the molecular epidemiological characteristics of NoV in children with AGE in Shanghai from 2018 to 2021.The overall detection rate of NoV was 11.9％(181/1545),with annual detection rates of 9.4％(36/381),13.6％(29/213),5.8％(13/226)and 14.2％(103/725),respectively.Of note,the prevalence of NoV in 2020 was significantly lower than that in 2018-2019(10.9％,65/594)(P=0.023)and 2021(14.2％,103/725)(P=0.000).The 181 NoV strains identified in this study were classified into the GⅠ group(1.1％,2/181),GⅡ group(98.3％,178/181)and GⅨ group(0.6％,1/181)according to the VP1 gene.The most common NoV VP1 genotype was GⅡ.4 Sydney_2012(63.5％,115/181),followed by GⅡ.3(19.9％,36/181)and GⅡ.2(9.4％,17/181).For P genotypes,174 strains were sequenced successfully according to the RdRp gene,and the predominant genotype was GⅡ.P16(44.8％,78/174),followed by GⅡ.P31(25.9％,45/174)and GⅡ.P12(21.3％,37/174).Among the 174 cases,GⅡ.4 Sydney_2012[P16](36.8％,64/174)was the dominant genotype,followed by GⅡ.4 Sydney_2012[P31](25.3％,44/174),GⅡ.3[P12](20.1％,35/174)and GⅡ.2[P1 6](8.0％,14/174).In particular,the dominant genotypes in Shanghai changed from GⅡ.4 Sydney_2012[P31]in 2018-2019 to GⅡ.4 Sydney_2012[P16]in 2020-2021.This is the first report to describe the epidemiological changes in NoV infection before and during the COVID-19 pandemic in Shanghai.These data highlight the importance of continuous surveillance for NoV in children with AGE in Shanghai.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    HBV precore G1896A mutation promotes growth of hepatocellular carcinoma cells by activating ERK/MAPK pathway

    Baoxin ZhaoHongxiu QiaoYan ZhaoZhiyun Gao...
    680-689页
    查看更多>>摘要：Chronic hepatitis B virus(HBV)infection is one of the leading causes of hepatocellular carcinoma(HCC).The HBV genome is prone to mutate and several variants are closely related to the malignant transformation of liver dis-ease.G1896A mutation(G to A mutation at nucleotide 1896)is one of the most frequently observed mutations in the precore region of HBV,which prevents HBeAg expression and is strongly associated with HCC.However,the mechanisms by which this mutation causes HCC are unclear.Here,we explored the function and molecular mechanisms of the G1896A mutation during HBV-associated HCC.G1896A mutation remarkably enhanced the HBV replication in vitro.Moreover,it increased tumor formation and inhibited apoptosis of hepatoma cells,and decreased the sensitivity of HCC to sorafenib.Mechanistically,the G1896A mutation could activate ERK/MAPK pathway to enhanced sorafenib resistance in HCC cells and augmented cell survival and growth.Collectively,our study demonstrates for the first time that the G1896A mutation has a dual regulatory role in exacerbating HCC severity and sheds some light on the treatment of G1896A mutation-associated HCC patients.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    miR-204 suppresses porcine reproductive and respiratory syndrome virus(PRRSV)replication via inhibiting LC3B-mediated autophagy

    Yao YaoSihan LiYingqi ZhuYangyang Xu...
    690-698页
    查看更多>>摘要：Porcine reproductive and respiratory syndrome(PRRS)caused by PRRS virus(PRRSV)has been regarded as a persistent challenge for the swine farms worldwide.microRNAs(miRNAs)play key roles in regulating almost every important biological process,including virus-host interaction.In this study,we found that miR-204 was highly expressed in cells that were not permissive to PRRSV infection compared with cells susceptible to PRRSV infection.Subsequently,we demonstrated that overexpression of miR-204 significantly inhibited PRRSV repli-cation in porcine alveolar macrophages(PAMs).Through bioinformatic analysis,we found that there existed a potential binding site of miR-204 on the 3'UTR of microtubule associated protein 1 light chain 3B(MAP1LC3B,LC3B),a hallmark of autophagy.Applying experiments including luciferase reporter assay and UV cross-linking and immunoprecipitation(CLIP)assay,we demonstrated that miR-204 directly targeted LC3B,thereby down-regulating autophagy.Meanwhile,we investigated the interplay between autophagy and PRRSV replication in PAMs,confirming that PRRSV infection induces autophagy,which in turn facilitates viral replication.Overall,we verify that miR-204 suppresses PRRSV replication via inhibiting LC3B-mediated autophagy in PAMs.These findings will provide a novel potential approach for us to develop antiviral therapeutic agents and controlling measures for future PRRSV outbreaks.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Long noncoding RNA 1392 regulates MDA5 by interaction with ELAVL1 to inhibit coxsackievirus B5 infection

    Jing LiJinwei LiPeiying TengFan Yang...
    699-708页
    查看更多>>摘要：Long noncoding RNAs(lncRNAs)modulate many aspects of biological and pathological processes.Recent studies have shown that host lncRNAs participate in the antiviral immune response,but functional lncRNAs in cox-sackievirus B5(CVB5)infection remain unknown.Here,we identified a novel cytoplasmic lncRNA,LINC1392,which was highly inducible in CVB5 infected RD cells in a time-and dose-dependent manner,and also can be induced by the viral RNA and IFN-β.Further investigation showed that LINC1392 promoted several important interferon-stimulated genes(ISGs)expression,including IFIT1,IFIT2,and IFITM3 by activating MDA5,thereby inhibiting the replication of CVB5 in vitro.Mechanistically,LINC1392 bound to ELAV like RNA binding protein 1(ELAVL1)and blocked ELAVL1 interaction with MDA5.Functional study revealed that the 245-835 nt locus of LINC1392 exerted the antiviral effect and was also an important site for ELAVL1 binding.In mice,LINC1392 could inhibit CVB5 replication and alleviated the histopathological lesions of intestinal and brain tissues induced by viral infection.Our findings collectively reveal that the novel LINC1392 acts as a positive regulator in the IFN-I signaling pathway against CVB5 infection.Elucidating the underlying mechanisms on how lncRNA regulats the host innate immunity response towards CVB5 infection will lay the foundation for antiviral drug research.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Autophagy induced by human adenovirus B7 structural protein Ⅵ inhibits viral replication

    Linlin ZhangYali DuanWei WangQi Li...
    709-722页
    查看更多>>摘要：Human adenovirus B7(HAdV-B7)causes severe acute lower respiratory tract infections in children.However,neither the child-specific antivirals or vaccines are available,nor the pathogenesis is clear.Autophagy,as part of innate immunity,plays an important role in resistance to viral infection by degrading the virus and promoting the development of innate and adaptive immunity.This study provided evidence that HAdV-B7 infection induced complete autophagic flux,and the pharmacological induction of autophagy decreased HAdV-B7 replication.In this process,the host protein Bcl2-associated athanogene 3(BAG3)mediated autophagy to inhibit the replication of HAdV-B7 by binding to the PPSY structural domain of viral protein pⅥ through its WW structural domain.These findings further our understanding of the host immune response during viral infection and will help to develop broad anti-HAdV therapies.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Inactivated SARS-CoV-2 booster vaccine enhanced immune responses in patients with chronic liver diseases

    Yongmei LiuJianhua LuHaoting ZhanWenfang Yuan...
    723-734页
    查看更多>>摘要：Chronic liver disease(CLD)entails elevated risk of COVID-19 severity and mortality.The effectiveness of the booster dose of inactivated SARS-CoV-2 vaccine in stimulating antibody response in CLD patients is unclear.Therefore,we conducted a cross-sectional study involving 237 adult CLD patients and 170 healthy controls(HC)to analyze neutralizing antibodies(NAbs)against SARS-CoV-2 prototype and BA.4/5 variant,anti-receptor binding domain(RBD)IgG,and total anti-SARS-CoV-2 antibodies.Serum levels of the total anti-SARS-CoV-2 antibodies,anti-RBD IgG and inhibition efficacy of NAbs were significantly elevated in CLD patients after the booster dose compared with the pre-booster dose,but were relatively lower than those of HCs.Induced humoral responses decreased over time after booster vaccination.The neutralization efficiency of the serum against BA.4/5 increased but remained below the inhibition threshold.All four SARS-CoV-2 antibodies,including total anti-SARS-CoV-2 antibodies,anti-RBD IgG and NAbs against prototype and BA.4/5,were lower in patients with severe CLD than those with non-severe CLD.After booster shot,age and time after the last vaccine were the risk factors for seropositivity of NAb against BA.4/5 in CLD patients.Additionally,white blood cell counts and hepatitis B core antibodies were the protective factors,and severe liver disease was the risk factor associated with seropositivity of total anti-SARS-CoV-2 antibodies.Overall,our data uncovered that antibody responses were improved in CLD patients and peaked at 120 days after the booster vaccines.All antibodies excepting total anti-SARS-CoV-2 antibodies declined after peak.CLD patients exhibited impaired immunologic responses to vaccination and weakened NAbs against BA.4/5,which hindered the protective effect of the booster shot against Omicron prevalence.Cellular immune responses should be further evaluated to determine the optimal vaccine regimen for CLD patients.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Abnormal liver function in children hospitalized with acute respiratory infection of adenoviruses:a retrospective study

    Xingui TianXiao LiShuyan QiuRong Zhou...
    735-740页
    查看更多>>摘要：Human adenoviruses(HAdVs)can cause acute hepatitis in immunocompromised patients.However,it is unclear whether HAdVs are contributors to hepatitis in immunocompetent children.In this study,the liver function test(LFT)results were retrospectively analyzed among children hospitalized(age＜14 years)between January 2016 and October 2019 for acute respiratory infection caused by adenoviruses.Alanine transaminase(ALT)and aspartate aminotransferase(AST)levels were elevated in 7.74％and 46.89％of patients,respectively.All patients with＞2 folds of the upper limit of ALT or AST levels were infected with HAdV-7 or HAdV-55.Significantly higher levels of ALT,AST,γ-glutamyl transpeptidase(γ-GT),and lower albumin levels were observed in the HAdV-7 infection group than in the HAdV-3 infection group.HAdV-55 infection led to significantly higher y-GT,total bilirubin,and direct bilirubin levels than the other infection types.The records of four patients with serial monitoring of the LFT results were further analyzed.Multiple indicators remained abnormal during the entire hospitalization in these patients.These results indicate that HAdV infection is often accompanied by abnormal liver function,and HAdV-7 and HAdV-55 might be under-recognized contributors to hepatitis among children.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis

    Yue SiHaijun ZhangZiqing ZhouXudong Zhu...
    741-754页
    查看更多>>摘要：Hantaan virus(HTNV)is a rodent-borne virus that causes hemorrhagic fever with renal syndrome(HFRS),resulting in a high mortality rate of 15％.Interferons(IFNs)play a critical role in the anti-hantaviral immune response,and IFN pretreatment efficiently restricts HTNV infection by triggering the expression of a series of IFN-stimulated genes(ISGs)through the Janus kinase-signal transducer and activator of transcription 1(JAK-STAT)pathway.However,the tremendous amount of IFNs produced during late infection could not restrain HTNV replication,and the mechanism remains unclear.Here,we demonstrated that receptor-interacting protein kinase 3(RIPK3),a crucial molecule that mediates necroptosis,was activated by HTNV and contributed to hantavirus evasion of IFN responses by inhibiting STAT1 phosphorylation.RNA-seq analysis revealed the upregulation of multiple cell death-related genes after HTNV infection,with RIPK3 identified as a key modulator of viral repli-cation.RIPK3 ablation significantly enhanced ISGs expression and restrained HTNV replication,without affecting the expression of pattern recognition receptors(PRRs)or the production of type Ⅰ IFNs.Conversely,exogenously expressed RIPK3 compromised the host's antiviral response and facilitated HTNV replication.RIPK3-/-mice also maintained a robust ability to clear HTNV with enhanced innate immune responses.Mechanistically,we found that RIPK3 could bind STAT1 and inhibit STAT1 phosphorylation dependent on the protein kinase domain(PKD)of RIPK3 but not its kinase activity.Overall,these observations demonstrated a noncanonical function of RIPK3 during viral infection and have elucidated a novel host innate immunity evasion strategy utilized by HTNV.
      原文链接:
    • NETL
    • NSTL
    • 万方数据