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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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    Antibiotic-induced gut bacteria depletion has no effect on HBV replication in HBV immune tolerance mouse model

    Yanan BuKaitao ZhaoZaichao XuYingcheng Zheng...
    335-343页
    查看更多>>摘要：Commensal microbiota is closely related to Hepatitis B virus(HBV)infection.Gut bacteria maturation accelerates HBV immune clearance in hydrodynamic injection(HDI)HBV mouse model.However,the effect of gut bacteria on HBV replication in recombinant adeno-associated virus(AAV)-HBV mouse model with immune tolerance remains obscure.We aim to investigate its role on HBV replication in AAV-HBV mouse model.C57BL/6 mice were administrated with broad-spectrum antibiotic mixtures(ABX)to deplete gut bacteria and intravenously injected with AAV-HBV to establish persistent HBV replication.Gut microbiota community was analyzed by fecal qPCR assay and 16S ribosomal RNA(rRNA)gene sequencing.HBV replication markers in blood and liver were determined by ELISA,qPCR assay and Western blot at indicated time points.Immune response in AAV-HBV mouse model was activated through HDI of HBV plasmid or poly(I∶C)and then detected by quantifying the percentage of IFN-γ+/CD8+T cells in the spleen via flow cytometry as well as the splenic IFN-γ mRNA level via qPCR assay.We found that antibiotic exposure remarkably decreased gut bacteria abundance and diversity.Antibiotic treatment failed to alter the levels of serological HBV antigens,intrahepatic HBV RNA transcripts and HBc protein in AAV-HBV mouse model,but contributed to HBsAg increase after breaking of immune tolerance.Overall,our data uncovered that antibiotic-induced gut bacteria depletion has no effect on HBV replication in immune tolerant AAV-HBV mouse model,providing new thoughts for elucidating the correlation between gut bacteria dysbiosis by antibiotic abuse and clinical chronic HBV infection.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    A novel bat coronavirus with a polybasic furin-like cleavage site

    Wentao ZhuYuyuan HuangJian GongLingzhi Dong...
    344-350页
    查看更多>>摘要：The current pandemic of COVID-19 caused by a novel coronavirus,severe acute respiratory syndrome coronavirus-2(SARS-CoV-2),threatens human health around the world.Of particular concern is that bats are recognized as one of the most potential natural hosts of SARS-CoV-2;however,coronavirus ecology in bats is still nascent.Here,we performed a degenerate primer screening and next-generation sequencing analysis of 112 bats,collected from Hainan Province,China.Three coronaviruses,namely bat betacoronavirus(Bat CoV)CD35,Bat CoV CD36 and bat alpha-coronavirus CD30 were identified.Bat CoV CD35 genome had 99.5％identity with Bat CoV CD36,both sharing the highest nucleotide identity with Bat Hp-betacoronavirus Zhejiang2013(71.4％),followed by SARS-CoV-2(54.0％).Phylogenetic analysis indicated that Bat CoV CD35 formed a distinct clade,and together with Bat Hp-betacoronavirus Zhejiang2013,was basal to the lineage of SARS-CoV-1 and SARS-CoV-2.Notably,Bat CoV CD35 harbored a canonical furin-like S1/S2 cleavage site that resembles the corresponding sites of SARS-CoV-2.The furin cleavage sites between CD35 and CD36 are identical.In addition,the receptor-binding domain of Bat CoV CD35 showed a highly similar structure to that of SARS-CoV-1 and SARS-CoV-2,especially in one binding loop.In conclusion,this study deepens our understanding of the diversity of coronaviruses and provides clues about the natural origin of the furin cleavage site of SARS-CoV-2.
      原文链接:
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    Epidemiology and genetic diversity of norovirus GⅡ genogroups among children in Hubei,China,2017-2019

    Jing LiLingyao ZhangWenjing ZouZhaohui Yang...
    351-362页
    查看更多>>摘要：Norovirus(NoV)is an important cause of viral acute gastroenteritis(AGE).To gain insights into the epidemio-logical characteristics and genetic diversity of NoV among children in Hubei,1216 stool samples from children(≤ 5 years)obtained under AGE surveillance from January 2017 to December 2019 were analyzed.The results showed that NoV was responsible for 14.64％of AGE cases,with the highest detection rate in children aged 7-12 months(19.76％).Statistically significant differences were found between male and female infection rates(x2=8.108,P=0.004).Genetic analysis of RdRp and VP1 sequences showed that NoV GⅡ genotypes were GⅡ.4 Sydney[P31](34.35％),GⅡ.3[P12](25.95％),GⅡ.2[P16](22.90％),GⅡ.4 Sydney[P16](12.98％),GⅡ.17[P17](2.29％),GⅡ.6[P7]and GⅡ.3[P16](each at 0.76％).GⅡ.17[P17]variants were divided into the Kawasaki323-like lineage and the Kawasaki308-like lineage.A unique recombination event was detected between strains of GⅡ.4 Sydney 2012 and GⅡ.4 Sydney 2016.Significantly,all GⅡ.P16 sequences associated with GⅡ.4/GⅡ.2 ob-tained in Hubei were correlated with novel GⅡ.2[P16]variants that re-emerged in Germany in 2016.Antigenic site analysis of complete VP1 sequences from all GⅡ.4 variants from Hubei identified notable variable residues of antibody epitopes.Genotyping under continuous AGE surveillance and observation of the antigenic sites of VP1 are important monitoring strategies for emerging NoV strains.
      原文链接:
    • NETL
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    Prevalence,variation,and transmission patterns of human respiratory syncytial virus from pediatric patients in Hubei,China during 2020-2021

    Yi YanDecheng WangYing LiZhiyong Wu...
    363-372页
    查看更多>>摘要：Human respiratory syncytial virus(RSV)is a severe threat to children and a main cause of acute lower respiratory tract infections.Nevertheless,the intra-host evolution and inter-regional diffusion of RSV are little known.In this study,we performed a systematic surveillance in hospitalized children in Hubei during 2020-2021,in which 106 RSV-positive samples were detected both clinically and by metagenomic next generation sequencing(mNGS).RSV-A and RSV-B groups co-circulated during surveillance with RSV-B being predominant.About 46 high-quality genomes were used for further analyses.A total of 163 intra-host nucleotide variation(iSNV)sites distributed in 34 samples were detected,and glycoprotein(G)gene was the most enriched gene for iSNVs,with non-synonymous substitutions more than synonymous substitutions.Evolutionary dynamic analysis showed that the evolutionary rates of G and NS2 genes were higher,and the population size of RSV groups changed over time.We also found evidences of inter-regional diffusion from Europe and Oceania to Hubei for RSV-A and RSV-B,respectively.This study highlighted the intra-host and inter-host evolution of RSV,and provided some evi-dences for understanding the evolution of RSV.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Construction and characterization of a synthesized herpes simplex virus H129-Syn-G2

    Han XiaoHengrui HuYijia GuoJiang Li...
    373-379页
    查看更多>>摘要：Herpes simplex virus type 1(HSV-1)causes lifelong infections worldwide,and currently there is no efficient cure or vaccine.HSV-1-derived tools,such as neuronal circuit tracers and oncolytic viruses,have been used exten-sively;however,further genetic engineering of HSV-1 is hindered by its complex genome structure.In the present study,we designed and constructed a synthetic platform for HSV-1 based on H129-G4.The complete genome was constructed from 10 fragments through 3 rounds of synthesis using transformation-associated recombination(TAR)in yeast,and was named H129-Syn-G2.The H129-Syn-G2 genome contained two copies of the gfp gene and was transfected into cells to rescue the virus.According to growth curve assay and electron microscopy results,the synthetic viruses exhibited more optimized growth properties and similar morphogenesis compared to the parental virus.This synthetic platform will facilitate further manipulation of the HSV-1 genome for the devel-opment of neuronal circuit tracers,oncolytic viruses,and vaccines.
      原文链接:
    • NETL
    • NSTL
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    Deletion of the first glycosylation site promotes Lassa virus glycoprotein-mediated membrane fusion

    Siqi DongWenting MaoYang LiuXiaoying Jia...
    380-386页
    查看更多>>摘要：The Lassa virus(LASV)is endemic in West Africa and causes severe hemorrhagic Lassa fever in humans.The glycoprotein complex(GPC)of LASV is highly glycosylation-modified,with 11 N-glycosylation sites.All 11 N-linked glycan chains play critical roles in GPC cleavage,folding,receptor binding,membrane fusion,and immune evasion.In this study,we focused on the first glycosylation site because its deletion mutant(N79Q)results in an unexpected enhanced membrane fusion,whereas it exerts little effect on GPC expression,cleavage,and receptor binding.Meanwhile,the pseudotype virus bearing GPCN79Q was more sensitive to the neutralizing antibody 37.7H and was attenuated in virulence.Exploring the biological functions of the key glycosylation site on LASV GPC will help elucidate the mechanism of LASV infection and provide strategies for the development of attenuated vaccines against LASV infection.
      原文链接:
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    • NSTL
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    3Cpro of FMDV inhibits type Ⅱ interferon-stimulated JAK-STAT signaling pathway by blocking STAT1 nuclear translocation

    Xiangju WuLei ChenChao SuiYue Hu...
    387-397页
    查看更多>>摘要：Foot-and-mouth disease virus(FMDV)has developed various strategies to antagonize the host innate immunity.FMDV Lpro and 3Cpro interfere with type Ⅰ IFNs through different mechanisms.The structural protein VP3 of FMDV degrades Janus kinase 1 to suppress IFN-γ signaling transduction.Whether non-structural proteins of FMDV are involved in restraining type Ⅱ IFN signaling pathways is unknown.In this study,it was shown that FMDV replication was resistant to IFN-γ treatment after the infection was established and FMDV inhibited type Ⅱ IFN induced expression of IFN-γ-stimulated genes(ISGs).We also showed for the first time that FMDV non-structural protein 3C antagonized IFN-γ-stimulated JAK-STAT signaling pathway by blocking STAT1 nuclear translocation.3Cpro expression significantly reduced the ISGs transcript levels and palindromic gamma-activated sequences(GAS)promoter activity,without affecting the protein level,tyrosine phosphorylation,and homodimerization of STAT1.Finally,we provided evidence that 3C protease activity played an essential role in degrading KPNA1 and thus inhibited ISGs mRNA and GAS promoter activities.Our results reveal a novel mechanism by which an FMDV non-structural protein antagonizes host type Ⅱ IFN signaling.
      原文链接:
    • NETL
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    Transcriptome analysis of CD4 T cells from HIV-infected individuals receiving ART with LLV revealed novel transcription factors regulating HIV-1 promoter activity

    Jingliang ChenYaozu HeHuolin ZhongFengyu Hu...
    398-408页
    查看更多>>摘要：Some HIV-infected individuals receiving ART develop low-level viremia(LLV),with a plasma viral load of 50-1000 copies/mL.Persistent low-level viremia is associated with subsequent virologic failure.The peripheral blood CD4+T cell pool is a source of LLV.However,the intrinsic characteristics of CD4+T cells in LLV which may contribute to low-level viremia are largely unknown.We analyzed the transcriptome profiling of peripheral blood CD4+T cells from healthy controls(HC)and HIV-infected patients receiving ART with either virologic sup-pression(VS)or LLV.To identify pathways potentially responding to increasing viral loads from HC to VS and to LLV,KEGG pathways of differentially expressed genes(DEGs)were acquired by comparing VS with HC(VS-HC group)and LLV with VS(LLV-VS group),and overlapped pathways were analyzed.Characterization of DEGs in key overlapping pathways showed that CD4+T cells in LLV expressed higher levels of Th1 signature transcription factors(TBX21),toll-like receptors(TLR-4,-6,-7 and-8),anti-HIV entry chemokines(CCL3 and CCL4),and anti-IL-1β factors(ILRN and IL1R2)compared to VS.Our results also indicated activation of the NF-κB and TNF signaling pathways that could promote HIV-1 transcription.Finally,we evaluated the effects of 4 and 17 tran-scription factors that were upregulated in the VS-HC and LLV-VS groups,respectively,on HIV-1 promoter activity.Functional studies revealed that CXXC5 significantly increased,while SOX5 markedly suppressed HIV-1 tran-scription.In summary,we found that CD4+T cells in LLV displayed a distinct mRNA profiling compared to that in VS,which promoted HIV-1 replication and reactivation of viral latency and may eventually contribute to virologic failure in patients with persistent LLV.CXXC5 and SOX5 may serve as targets for the development of latency-reversing agents.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    FOLR1-induced folate deficiency reduces viral replication via modulating APOBEC3 family expression

    Jing WuYajing HanRuining LyuFang Zhang...
    409-418页
    查看更多>>摘要：Folate receptor alpha(FOLR1)is vital for cells ingesting folate(FA).FA plays an indispensable role in cell pro-liferation and survival.However,it is not clear whether the axis of FOLR1/FA has a similar function in viral replication.In this study,we used vesicular stomatitis virus(VSV)to investigate the relationship between FOLR1-mediated FA deficiency and viral replication,as well as the underlying mechanisms.We discovered that FOLR1 upregulation led to the deficiency of FA in HeLa cells and mice.Meanwhile,VSV replication was notably sup-pressed by FOLR1 overexpression,and this antiviral activity was related to FA deficiency.Mechanistically,FA deficiency mainly upregulated apolipoprotein B mRNA editing enzyme catalytic subunit 3B(APOBEC3B)expression,which suppressed VSV replication in vitro and in vivo.In addition,methotrexate(MTX),an FA metabolism inhibitor,effectively inhibited VSV replication by enhancing the expression of APOBEC3B in vitro and in vivo.Overall,our present study provided a new perspective for the role of FA metabolism in viral infections and highlights the potential of MTX as a broad-spectrum antiviral agent against RNA viruses.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    TRAF7 negatively regulates the RLR signaling pathway by facilitating the K48-linked ubiquitination of TBK1

    Jing-Ping HuangYa-Xian YangTian ChenDan-Dan Wang...
    419-428页
    查看更多>>摘要：TANK-binding kinase 1(TBK1)is a nodal protein involved in multiple signal transduction pathways.In RNA virus-mediated innate immunity,TBK1 is recruited to the prion-like platform formed by MAVS and subsequently activates the transcription factors IRF3/7 and NF-κB to produce type Ⅰ interferon(IFN)and proinflammatory cytokines for the signaling cascade.In this study,TRAF7 was identified as a negative regulator of innate immune signaling.TRAF7 interacts with TBK1 and promotes K48-linked polyubiquitination and degradation of TBK1 through its RING domain,impairing the activation of IRF3 and the production of IFN-p.In addition,we found that the conserved cysteine residues at position 131 of TRAF7 are necessary for its function toward TBK1.Knockout of TRAF7 could facilitate the activation of IRF3 and increase the transcript levels of downstream antiviral genes.These data suggest that TRAF7 negatively regulates innate antiviral immunity by promoting the K48-linked ubiquitination of TBK1.
      原文链接:
    • NETL
    • NSTL
    • 万方数据