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Journal of Integrative Agriculture 2024年第4期23卷 1274-1284页

作者： Wei Zhang Shaoyang Li Rong Li Jinzhi Niu Jinjun Wang Key Laboratory of Entomology and Pest Control Engineering College of Plant ProtectionSouthwest UniversityChongqing 400715China Key Laboratory of Agricultural Biosafety and Green Production of Upper Yangtze River Ministry of Education/International Joint Laboratory of China-Belgium on Sustainable Crop Pest ControlAcademy of Agricultural SciencesSouthwest UniversityChongqing 400715China

The Janus kinase/signal transducers and activators of transcription(JAK/STAT)signaling pathway play a pivotal role in innate immunity.Among invertebrates,Domeless receptors serve as the key upstream regulators of this pathway.In our study on Bactrocera dorsalis,we identified three cytokine receptors:BdDomeless1,BdDomeless2,and BdDomeless3.Each receptor encompasses five fibronectin-type-III-like(FN III)extracellular domains and a transmembrane domain.Furthermore,these receptors exhibit the increased responsiveness to diverse pathogenic challenges.Notably,only BdDomeless3 is upregulated during symbiont-like viral infections.Moreover,silencing BdDomeless3 enhanced the infectivity of Bactrocera dorsalis cripavirus(BdCV)and B.dorsalis picorna-like virus(BdPLV),underscoring BdDomeless3’s crucial role in antiviral defense of B.dorsalis.Following the suppression of Domeless3 expression,six antimicrobial peptide genes displayed decreased expression,potentially correlating with the rise in viral infectivity.To our knowledge,this is the first study identifying cytokine receptors associated with the JAK/STAT pathway in tephritid flies,shedding light on the immune mechanisms of B.dorsalis.

关键词： Bactrocera dorsalis JAK/STAT pathway Domeless receptors antiviral immunity symbiont-like virus

Coronavirus membrane-associated papain-like proteases induce autophagy through interacting with Beclinl to negatively regulate antiviral innate immunity

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Protein & Cell 2014年第12期5卷 912-927页

作者： Xiaojuan Chen Kai Wang Yaling Xing Jian Tu Xingxing Yang Qian Zhao Kui Li Zhongbin Chen Division of Infection and immunity Department of Electromagnetic and Laser Biology Beijing Institute of Radiation Medicine Beijing 100850 China Department of Immunology Bengbu Medical College Bengbu 233030 China Prince of Wales Clinical School The University of New South Wales Sydney NSW 2052 Australia Department of Microbiology Immunology and Biochemistry University of Tennessee Health Science Center Memphis TN 38163 USA

Autophagy plays important roles in modulating viral replication and antiviral immune response. Coronavirus infection is associated with the autophagic process, however, little is known about the mechanisms of autophagy induction and its contribution to coronavirus regulation of host innate responses. Here, we show that the membrane-associated papain-like protease PLP2 （PLP2-TM） of coronaviruses acts as a novel autophagy- inducing protein. Intriguingly, PLP2-TM induces incom- plete autophagy process by increasing the accumula- tion of autophagosomes but blocking the fusion of autophagosomes with lysosomes. Furthermore, PLP2- TM interacts with the key autophagy regulators, LC3 and Beclinl, and promotes Beclinl interaction with STING, the key regulator for antiviral IFN signaling. Finally, knockdown of Beclinl partially reverses PLP2-TM＇s inhibitory effect on innate immunity which resulting in decreased coronavirus replication. These results sug- gested that coronavirus papain-like protease induces incomplete autophagy by interacting with Beclinl, which in turn modulates coronavirus replication and antiviral innate immunity.

关键词： coronavirus papain-like proteaseautophagy antiviral immunity Beclinl STING

Sex differences in SARS-CoV-2 infections,anti-viral immunity and vaccine responses

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Asian Pacific Journal of Tropical Medicine 2022年第3期15卷 97-105页

作者： Abhishek Mohanty Aanchal Sawhney Shefali Gupta Vishal Rao Periyasamy Govindaraj Sambit Mohanty Vandana Jain Rajiv Gandhi Cancer Institute and Research Centre New DelhiIndia HCG Cancer Hospitals BangaloreIndia All India Institute of Medical Sciences Rae BareliIndia Centre for DNA Finger Printing and Diagnostics HyderabadIndia CORE Diagnostics GurgaonHaryanaIndia

The COVID-19 pandemic has revealed sex-based differences in anti-viral responses,with a higher rate of SARS-CoV-2 infections as well as a higher rate of morbidity and mortality in men than in women.Males and females also show disparate immune responses to COVID-19 infection,which may be important contributors to lower rates of infection,disease severity and deaths in women than in men.Here,the authors review sex differences in SARS-CoV-2 infections,anti-viral immunity and vaccine responses,putting forth the importance of sex,the underappreciated variables in vaccine response and disease infectivity.

关键词： SARS-CoV-2 antiviral immunity Sex based mitochondrial differences Vaccine responses Innate immunity Sex differences COVID-19 pandemic

ISG20 inhibits bluetongue virus replication

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Virologica Sinica 2022年第4期37卷 521-530页

作者： Di Kang Shandian Gao Zhancheng Tian Guorui Zhang Guiquan Guan Guangyuan Liu Jianxun Luo Junzheng Du Hong Yin State Key Laboratory of Veterinary Etiological Biology Lanzhou Veterinary Research InstituteChinese Academy of Agricultural SciencesLanzhou730046China Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses Yangzhou UniversityYangzhou225009China

ISG20 is an interferon-inducible exonuclease that inhibits virus replication.Although ISG20 is thought to degrade viral RNA,the antiviral mechanism and specificity of ISG20 remain unclear.In this study,the antiviral role of ovine ISG20(o ISG20)in bluetongue virus(BTV)infection was investigated.It was found that BTV infection upregulated the transcription of ovine ISG20(o ISG20)in a time-and BTV multiplicity of infection(MOI)-dependent manner.Overexpression of o ISG20 suppressed the production of BTV genome,proteins,and virus titer,whereas the knockdown of o ISG20 increased viral replication.o ISG20 was found to co-localize with BTV proteins VP4,VP5,VP6,and NS2,but only directly interacted with VP4.Exonuclease defective o ISG20 significantly decreased the inhibitory effect on BTV replication.In addition,the interaction of mutant o ISG20 and VP4 was weakened,suggesting that binding to VP4 was associated with the inhibition of BTV replication.The present data characterized the anti-BTV effect of o ISG20,and provides a novel clue for further exploring the inhibition mechanism of double-stranded RNA virus by ISG20.

关键词： Bluetongue virus(BTV) Interferon-stimulated genes(ISGs) Ovine ISG20 Virus replication antiviral immunity

Adaptive immunity in the liver

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Cellular & Molecular Immunology 2016年第3期13卷 354-368页

作者： Zongwen Shuai Miranda WY Leung Xiaosong He Weici Zhang Guoxiang Yang Patrick SC Leung M Eric Gershwin Division of Rheumatology Allergy and Clinical Immunology University of California Davis School of Medicine Davis CA 95616 USA Department of Rheumatology and Immunology The First Affiliated Hospital of Anhui Medical University Hefei 230022 China.

The anatomical architecture of the human liver and the diversity of its immune components endow the liver with its physiological function of immune competence. Adaptive immunity is a major arm of the immune system that is organized in a highly specialized and systematic manner, thus providing long-lasting protection with immunological memory. Adaptive immunity consists of humoral immunity and cellular immunity. Cellular immunity is known to have a crucial role in controlling infection, cancer and autoimmune disorders in the liver. In this article, we will focus on hepatic virus infections, hepatocellular carcinoma and autoimmune disorders as examples to illustrate the current understanding of the contribution of T cells to cellular immunity in these maladies. Cellular immune suppression is primarily responsible for chronic viral infections and cancer. However, an uncontrolled auto-reactive immune response accounts for autoimmunity. Consequently, these immune abnormalities are ascribed to the quantitative and functional changes in adaptive immune cells and their subsets, innate immunocytes, chemokines, cytokines and various surface receptors on immune cells. A greater understanding of the complex orchestration of the hepatic adaptive immune regulators during homeostasis and immune competence are much needed to identify relevant targets for clinical intervention to treat immunological disorders in the liver.

关键词： adaptive immunity T cells immunopathogenesis antiviral immunity

Coronavirus papain-like proteases induce incomplete autophagy through interacting with Beclin 1 to negatively regulate antiviral innate immunity

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Coronavirus papain-like proteases induce incomplete autophag...

Virus-induced E3 ligase FBXW7 nuclear export is critical for RIG-I stabilization in antiviral immunity

第九届全国免疫学学术大会

作者： Zhongbin Chen Xiaojuan Chen Kai Wang Yaling Xing Xingxing Yang Qian Zhao Beijing Institute of Radiation Medicine

Autophagy plays important roles in modulating viral replication and antiviral immune response.Coronavirus infection is associated with the autophagic process,however,little is known about the mechanisms of autophagy induction and its contribution to coronavirus regulation of host innate responses.Here,we show that the membrane-associated papain-like protease PLP2(PLP2-TM)of coronaviruses acts as a novel autophagy-inducing protein.Intriguingly,PLP2-TM induces incomplete autophagy process by increasing the accumulation of autophagosomes but blocking the fusion of autophagosomes with lysosomes.Furthermore,PLP2-TM interacts with the key autophagy regulators,LC3 and Beclinl,and promotes Beclinl interaction with STING,the key regulator for antiviral IFN signaling.Finally,Knockdown of Beclin 1partially reverses PLP2-TM’s inhibitory effect on innate immunity which resulting in decreased coronavirus replication.These results suggested that coronavirus papain-like protease induces incomplete autophagy by interacting with Beclin 1,which in turn modulates coronavirus replication and antiviral innate immunity.

关键词： Coronavirus Papain-like protease Autophagy antiviral immunity Beclinl STING

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Virus-induced E3 ligase FBXW7 nuclear export is critical for...

TRIM35 mediates protection against influenza infection by activating TRAF3 and degrading viral PB2

第十一届全国免疫学学术大会

作者： Song Yinjing Lai Lihua Chong Zhenlu He Jia Zhang Yuanyuan Liu Yang Wang Qingqing Institute of Immunology Zhejiang University School of Medicine

Objective:To study the function and mechanisms of E3 ligase FBXW7 in antiviral immunity.Materials and Methods:The FBXW7 m RNA expression in the peripheral blood mononuclear cells(PBMCs)from70 cases of patients infected with respiratory syncytial virus(RSV)and control healthy children was detected by QPCR.FBXW7 si RNA and Lysm+FBXW7f/f mice were utilized to detect the function of FBXW7 in antiviral immunity.

关键词： E3 ligase FBXW7 nuclear export RIG-I stabilization antiviral immunity SHP-2

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Protein & Cell 2020年第12期11卷 894-914页

作者： Nan Sun Li Jiang Miaomiao Ye Yihan Wang Guangwen Wang Xiaopeng Wan Yuhui Zhao Xia Wen Libin Liang Shujie Ma Liling Liu Zhigao Bu Hualan Chen Chengjun Li State Key Laboratory of Veterinary Biotechnology Harbin Veterinary Research InstituteChinese Academy of Agricultural SciencesHarbin 150069China

Tripartite motif(TRIM)family proteins are important effectors of innate immunity against viral infections.Here we identified TRIM35 as a regulator of TRAF3 activation.Deficiency in or inhibition of TRIM35 suppressed the production of type I interferon(IFN)in response to viral infection.777m35-deficient mice were more susceptible to influenza A virus(IAV)infection than were wild-type mice.TRIM35 promoted the RIG-Imediated signaling by catalyzing Lys63-linked polyubiquitination of TRAF3 and the subsequent formation of a signaling complex with VISA and TBK1.IAV PB2 polymerase countered the innate antiviral immune response by impeding the Lys63-linked polyubiquitination and activation of TRAF3.TRIM35 mediated Lys48-linked polyubiquitination and proteasomal degradation of IAV PB2,thereby antagonizing its suppression of TRAF3 activation.Our in vitro and in vivo findings thus reveal novel roles of TRIM35,through catalyzing Lys63-or Lys48-linked polyubiquitination,in RIG-I antiviral immunity and mechanism of defense against IAV infection.

关键词： influenza A virus PB2 TRIM35 TRAF3 ubiquitination antiviral immunity

SARS-CoV-2 nsp12 attenuates type Ⅰ interferon production by inhibiting IRF3 nuclear translocation

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Cellular & Molecular Immunology 2021年第4期18卷 945-953页

作者： Wenjing Wang Zhuo Zhou Xia Xiao Zhongqin Tian Xiaojing Dong Conghui Wang Li Li Lili Ren Xiaobo Lei Zichun Xiang Jianwei Wang NHC Key Laboratory of System Biology of Pathogens Institute of Pathogen BiologyChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100730PR China Key Laboratory of Respiratory Disease Pathogenomics Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730PR China Christophe Merieux Laboratory Institute of Pathogen BiologyChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100730PR China Biomedical Pioneering Innovation Center Beijing Advanced Innovation Center for GenomicsPeking University Genome Editing Research CenterSchool of Life SciencesPeking UniversityBeijing 100871China

SARS-CoV-2 is the pathogenic agent of COVID-19,which has evolved into a global pandemic.Compared with some other respiratory RNA viruses,SARS-CoV-2 is a poor inducer of type Ⅰ interferon(IFN).Here,we report that SARS-CoV-2 nsp12,the viral RNA-dependent RNA polymerase(RdRp),suppresses host antiviral responses.SARS-CoV-2 nsp12 attenuated Sendai virus(SeV)-or poly(I:C)-induced IFN-β promoter activation in a dose-dependent manner.It also inhibited IFN promoter activation triggered by RIG-I,MDA5,MAVS,and IRF3 overexpression.Nsp12 did not impair IRF3 phosphorylation but suppressed the nuclear translocation of IRF3.Mutational analyses suggested that this suppression was not dependent on the polymerase activity of nsp12.Given these findings,our study reveals that SARS-CoV-2 RdRp can antagonize host antiviral innate immunity and thus provides insights into viral pathogenesis.

关键词： SARS-CoV-2 COVID-19 Nsp12 antiviral immunity

The immune tolerant phase of chronic HBV infection： new perspectives on an old concept

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Cellular & Molecular Immunology 2015年第3期12卷 258-263页

作者： Antonio Bertoletti Patrick T Kennedy Emerging Infectious Diseases (EID) Program Duke-NUS Graduate Medical School Singapore Viral Hepatitis Laboratory Singapore Institute for ClinicalSciences Agency of Science Technology and Research (A＊STAR) Singapore and Blizard Institute Barts and The London School of Medicine & DentistryLondon UK

Chronic hepatitis B virus （HBV） infection progresses through distinct disease phases that are strongly associated with patient age. The so-called immune tolerant （IT） phase represents the classical early phase of infection; it is associated with high levels of HBV replication and lack of clinical signs of liver Inflammation. Whether this phase of HBV infection is also associated with immunological features of ＂tolerance＇ has recently been challenged. Here, we review the data that dispute this concept of immune tolerance and then propose an alternative interpretation of the immunopathological events that take place during this early phase of CHB infection.

关键词： Hepatitis B antiviral immunity T cells