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| 1 | Current status of severe fever with thrombocytopenia syndrome in China显示文摘Severe fever with thrombocytopenia syndrome(SFTS) is an emerging infectious disease caused by SFTS virus(SFTSV). SFTSV is associated with a high mortality rate and has been reported in China, South Korea and Japan. SFTSV undergoes rapid changes owing to evolution, gene mutations, and reassortment between different strains of SFTSV. In this review, we summarize the recent cases and general properties of SFTS, focusing on the epidemiology, genetic diversity,clinical features, and diagnostics of SFTSV in China. From 2010 to October 2016, SFTS cases were reported in 23 provinces of China, with increased numbers yearly. Infection and death cases are mainly found in central China, where the Haemaphysalis longicornis ticks are spread. The national average mortality rate of SFTS infection was 5.3%, with higher risk to elder people. The main epidemic period was from May to July, with a peak in May. Thus, SFTS reminds a significant public health problem, and development of prophylactic vaccines and effective antiviral drugs will be highly needed. | Jianbo Zhan Qin Wang Jing Cheng Bing Hu Jing Li Faxian Zhan Yi Song Deyin Guo | 2017 | Virologica Sinica2017，32，1： | 71 |
| 2 | Molecular mechanisms of coronavirus RNA capping and methylation显示文摘The 5′-cap structures of eukaryotic m RNAs are important for RNA stability, pre-m RNA splicing,m RNA export, and protein translation. Many viruses have evolved mechanisms for generating their own cap structures with methylation at the N7 position of the capped guanine and the ribose 2′-Oposition of the first nucleotide, which help viral RNAs escape recognition by the host innate immune system. The RNA genomes of coronavirus were identified to have 5′-caps in the early1980 s. However, for decades the RNA capping mechanisms of coronaviruses remained unknown.Since 2003, the outbreak of severe acute respiratory syndrome coronavirus has drawn increased attention and stimulated numerous studies on the molecular virology of coronaviruses. Here, we review the current understanding of the mechanisms adopted by coronaviruses to produce the 5′-cap structure and methylation modification of viral genomic RNAs. | Yu Chen Deyin Guo | 2016 | Virologica Sinica2016，31，1： | 14 |
| 3 | The functions of tumor suppressor PTEN in innate and adaptive immunity显示文摘The tumor suppressor phosphatase and tensin homolog(PTEN)is a lipid and protein phosphatase that is able to antagonize the PI3K/AKT pathway and inhibit tumor growth.PTEN also possesses phosphatase-independent functions.Genetic alterations of PTEN may lead to the deregulation of cell proliferation,survival,differentiation,energy metabolism and cellular architecture and mobility.Although the role of PTEN in tumor suppression is extensively documented and well established,the evidence for its roles in immunity did not start to accumulate until recently.In this review,we will focus on the newly discovered functions of PTEN in the regulation of innate and adaptive immunity,including antiviral responses. | Lang Chen Deyin Guo | 2017 | Cellular & Molecular Immunology2017，14，7： | 12 |
| 4 | A novel selective autophagy receptor,CCDC50,delivers K63 polyubiquitination-activated RIG-I/MDA5 for degradation during viral infection显示文摘Autophagy is a con served process that delivers cytosolic substa nces to the lysosome for degradatio n,but its direct role in the regulation of antiviral inn ate immu nity remains poorly un derstood.Here,through high-throughput screeni ng,we discovered that CCDC50 functions as a previously unknown autophagy receptor that negatively regulates the type I interferon(IFN)signaling pathway initiated by RIG-I-like receptors(RLRs),the sensors for RNA viruses.The expression of CCDC50 is enhanced by viral infection,and CCDC50 specifically recognizes K63-polyubiquitinated RLRs,thus delivering the activated RIG-I/MDA5 for autophagic degradation.The associatio n of CCDC50 with phagophore membrane protei n LC3 is con firmed by crystal structure analysis.In contrast to other known autophagic cargo receptors that associate with either the LIR-docking site(LDS)or the UIMdocking site(UDS)of LC3,CCDC50 can bind to both LDS and UDS,representing a new type of cargo receptor.In mouse models with RNA virus infection,CCDC50 deficiency reduces the autophagic degradation of RIG-I/MDA5 and promotes type I IFN responses,resulting in enhaneed viral resistance and improved survival rates.These results reveal a new link between autophagy and antiviral innate immune resp on ses and provide additional in sights into the regulatory mecha nisms of RLR-mediated antiviral signaling. | Panpan Hou Kongxiang Yang Penghui Jia Lan Liu Yuxin Lin Zibo Li Jun Li Shuliang Chen Shuting Guo Ji'An Pan Junyu Wu Hong Peng Weijie Zeng Chunmei Li Yingfang Liu Deyin Guo | 2021 | Cell Research2021，31，1： | 5 |
| 5 | PTEN-L promotes type I interferon responses and antiviral immunity显示文摘Phosphatase and tensin homolog deleted on chromosome ten(PTEN)is a well-known tumor suppressor that acts as a dual-specificity phosphatase and is frequently mutated in human cancer.Our previous work has demonstrated that PTEN also plays a vital role in type I interferon responses and antiviral innate immunity.Recently,a translational variant of PTEN with a long N-terminal extension(PTEN-L)has been discovered that is secreted into the extracellular environment and enters recipient cells,where it exerts a phosphatase function antagonistic to PI3K/Akt signaling and tumorigenesis.In this study,we demonstrate that PTEN-L promotes type I interferon responses and antiviral innate immunity during viral infection in a phosphatase activity-dependent manner.Compared with canonical PTEN,PTEN-L also exerts its antiviral function when it is applied exogenously in protein form.This finding was confirmed in cell cultures and mouse infection models.Furthermore,PTEN-L enhances the responses of both type I interferon and proinflammatory cytokines,thus suggesting that PTEN-L might possess additional functions compared with those of PTEN.Thus,the antiviral function of PTEN-L may open an avenue for the use of PTEN-L in antiviral therapy,particularly in patients with PTEN-deficient tumors. | Yuanyuan Cao Hongyun Wang Liu Yang Zhen Zhang Chenlin Li Xu Yuan Lang Bu Lang Chen Yu Chen Chun-Mei Li Deyin Guo | 2018 | Cellular & Molecular Immunology2018，15，1： | 3 |
| 6 | Autophagy receptor CCDC50 tunes the STING-mediated interferon response in viral infections and autoimmune diseases显示文摘DNA sensing and timely activation of interferon(IFN)-mediated innate immunity are crucial for the defense against DNA virus infections and the clearance of abnormal cells.However,overactivation of immune responses may lead to tissue damage and autoimmune diseases;therefore,these processes must be intricately regulated.STING is the key adaptor protein,which is activated by cyclic GMP-AMP,the second messenger derived from cGAS-mediated DNA sensing.Here,we report that CCDC50,a newly identified autophagy receptor,tunes STING-directed type I IFN signaling activity by delivering K63-polyubiquitinated STING to autolysosomes for degradation.Knockout of CCDC50 significantly increases herpes simplex virus 1(HSV-1)-or DNA ligand-induced production of type I IFN and proinflammatory cytokines.Ccdc50-deficient mice show increased production of IFN,decreased viral replication,reduced cell infiltration,and improved survival rates compared with their wild-type littermates when challenged with HSV-1.Remarkably,the expression of CCDC50 is downregulated in systemic lupus erythematosus(SLE),a chronic autoimmune disease.CCDC50 levels are negatively correlated with IFN signaling pathway activation and disease severity in human SLE patients.CCDC50 deficiency potentiates the cGAS-STING-mediated immune response triggered by SLE serum.Thus,our findings reveal the critical role of CCDC50 in the immune regulation of viral infections and autoimmune diseases and provide insights into the therapeutic implications of CCDC50 manipulation. | Panpan Hou Yuxin Lin Zibo Li Ruiqing Lu Yicheng Wang Tian Tian Penghui Jia Xi Zhang Liu Cao Zhongwei Zhou Chunmei Li Jieruo Gu Deyin Guo | 2021 | Cellular & Molecular Immunology2021，18，10： | 3 |
| 7 | Coronavirus: epidemiology, genome replication and the interactions with their hosts显示文摘This special issue of the journal is dedicated to the recent progress on coronaviruses and covers the topics of viral epidemiology,virus replication and the interactions between the coronaviruses and their hosts.Members of the family Coronaviridae infect a wide range of vertebrates and humans.They usually | Zheng-Li Shi Deyin Guo Peter J.M.Rottier | 2016 | Virologica Sinica2016，31，1： | 3 |
| 8 | A male-ABCD algorithm for hepatocellular carcinoma risk prediction in HBs Ag carriers显示文摘Objective: Hepatocellular carcinoma(HCC) development among hepatitis B surface antigen(HBs Ag) carriers shows gender disparity, influenced by underlying liver diseases that display variations in laboratory tests. We aimed to construct a risk-stratified HCC prediction model for HBs Ag-positive male adults.Methods: HBs Ag-positive males of 35-69 years old(N=6,153) were included from a multi-center populationbased liver cancer screening study. Randomly, three centers were set as training, the other three centers as validation. Within 2 years since initiation, we administrated at least two rounds of HCC screening using Bultrasonography and α-fetoprotein(AFP). We used logistic regression models to determine potential risk factors,built and examined the operating characteristics of a point-based algorithm for HCC risk prediction.Results: With 2 years of follow-up, 302 HCC cases were diagnosed. A male-ABCD algorithm was constructed including participant's age, blood levels of GGT(γ-glutamyl-transpeptidase), counts of platelets, white cells,concentration of DCP(des-γ-carboxy-prothrombin) and AFP, with scores ranging from 0 to 18.3. The area under receiver operating characteristic was 0.91(0.90-0.93), larger than existing models. At 1.5 points of risk score,26.10% of the participants in training cohort and 14.94% in validation cohort were recognized at low risk, with sensitivity of identifying HCC remained 100%. At 2.5 points, 46.51% of the participants in training cohort and 33.68% in validation cohort were recognized at low risk with 99.06% and 97.78% of sensitivity, respectively. At 4.5 points, only 20.86% of participants in training cohort and 23.73% in validation cohort were recognized at high risk,with positive prediction value of 22.85% and 12.35%, respectively.Conclusions: Male-ABCD algorithm identified individual's risk for HCC occurrence within short term for their HCC precision surveillance. | Yuting Wang Minjie Wang He Li Kun Chen Hongmei Zeng Xinyu Bi Zheng Zhu Yuchen Jiao Yong Wang Jian Zhu Hui Zhao Xiang Liu Chunyun Dai Chunsun Fan Can Zhao Deyin Guo Hong Zhao Jianguo Zhou Dongmei Wang Zhiyuan Wu Xinming Zhao Wei Cui Xuehong Zhang Jianqiang Cai Wanqing Chen Chunfeng Qu | 2021 | Chinese Journal of Cancer Research2021，33，3： | 3 |
| 9 | Mechanisms and Effects on HBV Replication of the Interaction between HBV Core Protein and Cellular Filamin B显示文摘Hepatitis B virus(HBV) infection is one of the major problems that threatens global health. There have been many studies on HBV, but the relationship between HBV and host factors is largely unexplored and more studies are needed to clarify these interactions. Filamin B is an actin-binding protein that acts as a cytoskeleton protein, and it is involved in cell development and several signaling pathways. In this study, we showed that filamin B interacted with HBV core protein,and the interaction promoted HBV replication. The interaction between filamin B and core protein was observed in HEK293T, Huh7 and HepG2 cell lines by co-immunoprecipitation and co-localization immnofluoresence. Overexpression of filamin B increased the levels of HBV total RNAs and pre-genome RNA(pg RNA), and improved the secretion level of hepatitis B surface antigen(HBsAg) and hepatitis B e antigen(HBeAg). In contrast, filamin B knockdown inhibited HBV replication, decreased the level of HBV total RNAs and pgRNA, and reduced the secretion level of HBsAg and HBeAg. In addition, we found that filamin B and core protein may interact with each other via four blocks of argentine residues at the C-terminus of core protein. In conclusion, we identify filamin B as a novel host factor that can interact with core protein to promote HBV replication in hepatocytes. Our study provides new insights into the relationship between HBV and host factors and may provide new strategies for the treatment of HBV infection. | Yilin Li Yishuang Sun Fuyun Sun Rong Hua Chenlin Li Lang Chen Deyin Guo Jingfang Mu | 2018 | Virologica Sinica2018，33，2： | 3 |
| 10 | Rapid isolation and immune profiling of SARS-CoV-2 specific memory B cell in convalescent COVID-19 patients via LIBRA-seq显示文摘B cell response plays a critical role against SARS-CoV-2 infection.However,little is known about the diversity and frequency of the paired SARS-CoV-2 antigen-specific BCR repertoire after SARS-CoV-2 infection.Here,we performed single-cell RNA sequencing and VDJ sequencing using the memory and plasma B cells isolated from five convalescent COVID-19 patients,and analyzed the spectrum and transcriptional heterogeneity of antibody immune responses.Via linking BCR to antigen specificity through sequencing(LIBRA-seq),we identified a distinct activated memory B cell subgroup(CD11c^(high) CD95^(high))had a higher proportion of SARS-CoV-2 antigen-labeled cells compared with memory B cells.Our results revealed the diversity of paired BCR repertoire and the non-stochastic pairing of SARS-CoV-2 antigen-specific immunoglobulin heavy and light chains after SARS-CoV-2 infection.The public antibody clonotypes were shared by distinct convalescent individuals.Moreover,several antibodies isolated by LIBRA-seq showed high binding affinity against SARS-CoV-2 receptor-binding domain(RBD)or nucleoprotein(NP)via ELISA assay.Two RBD-reactive antibodies C14646P3S and C2767P3S isolated by LIBRA-seq exhibited high neutralizing activities against both pseudotyped and authentic SARS-CoV-2 viruses in vitro.Our study provides fundamental insights into B cell response following SARS-CoV-2 infection at the single-cell level. | Bing He Shuning Liu Yuanyuan Wang Mengxin Xu Wei Cai Jia Liu Wendi Bai Shupei Ye Yong Ma Hengrui Hu Huicui Meng Tao Sun Yanling Li Huanle Luo Mang Shi Xiangjun Du Wenjing Zhao Shoudeng Chen Jingyi Yang Haipeng Zhu Yusheng Jie Yuedong Yang Deyin Guo Qiao Wang Yuwen Liu Huimin Yan Manli Wang Yao-Qing Chen | 2021 | Signal Transduction and Targeted Therapy2021，6，6： | 2 |
| 11 | A Convenient and Biosafe Replicon with Accessory Genes of SARS-CoV-2 and Its Potential Application in Antiviral Drug Discovery显示文摘SARS-CoV-2 causes the pandemic of COVID-19 and no effective drugs for this disease are available thus far.Due to the high infectivity and pathogenicity of this virus,all studies on the live virus are strictly confined in the biosafety level 3(BSL3)laboratory but this would hinder the basic research and antiviral drug development of SARS-CoV-2 because the BSL3 facility is not commonly available and the work in the containment is costly and laborious.In this study,we constructed a reverse genetics system of SARS-CoV-2 by assembling the viral cDNA in a bacterial artificial chromosome(BAC)vector with deletion of the spike(S)gene.Transfection of the cDNA into cells results in the production of an RNA replicon that keeps the capability of genome or subgenome replication but is deficient in virion assembly and infection due to the absence of S protein.Therefore,such a replicon system is not infectious and can be used in ordinary biological laboratories.We confirmed the efficient replication of the replicon by demonstrating the expression of the subgenomic RNAs which have similar profiles to the wild-type virus.By mutational analysis of nsp12 and nsp14,we showed that the RNA polymerase,exonuclease,and cap N7 methyltransferase play essential roles in genome replication and sgRNA production.We also created a SARS-CoV-2 replicon carrying a luciferase reporter gene and this system was validated by the inhibition assays with known anti-SARS-CoV-2 inhibitors.Thus,such a one-plasmid system is biosafe and convenient to use,which will benefit both fundamental research and development of antiviral drugs. | Yun-Yun Jin Hanwen Lin Liu Cao Wei-Chen Wu Yanxi Ji Liubing Du Yiling Jiang Yanchun Xie Kuijie Tong Fan Xing Fuxiang Zheng Mang Shi Ji-An Pan Xiaoxue Peng Deyin Guo | 2021 | Virologica Sinica2021，36，5： | 2 |
| 12 | PTEN suppresses tumorigenesis by directly dephosphorylating Akt显示文摘Dear Editor,The serine-threonine kinase Akt plays a central role in regulating cell proliferation,migration,angiogenesis,transformation,energy metabolism,and death.1 The stimulation of growth factors recruits the PI3K to the plasma membrane and phosphatidylinositol-3A5-trisphosphate(PIP3),which in turn recruits Akt to the plasma membrane through PH domain of Akt. | Lang Bu Huan Wang Ji-an Pan Lang Chen Fan Xing Junyu Wu Shun Li Deyin Guo | 2021 | Signal Transduction and Targeted Therapy2021，6，8： | 2 |
| 13 | Chimeric classical swine fever (CSF)-Japanese encephalitis (JE) viral replicon as a non-transmissible vaccine candidate against CSF and JE infections显示文摘 | Zhenhua Yang Rui Wu Robert W. Li Ling Li Zhongliang Xiong Haizhong Zhao Deyin Guo Zishu Pan | 2012 | Virus Research2012，，1： | 2 |
| 14 | Non-Structural Protein 5 of Zika Virus Interacts with p53 in Human Neural Progenitor Cells and Induces p53-Mediated Apoptosis显示文摘Zika virus(ZIKV) infection could disrupt neurogenesis and cause microcephaly in neonates by targeting neural progenitor cells(NPCs). The tumor suppressor p53-mediated cell cycle arrest and apoptotic cell death have been suggested to be activated upon ZIKV infection, yet the detailed mechanism is not well understood. In the present study, we investigated the effects of ZIKV-encoded proteins in the activation of p53 signaling pathway and found that, among the ten viral proteins,the nonstructural protein 5(NS5) of ZIKV most significantly activated the transcription of p53 target genes. Using the immunoprecipitation-coupled mass spectrometry approach, we identified that ZIKV-NS5 interacted with p53 protein. The NS5-p53 interaction was further confirmed by co-immunoprecipitation and GST pull-down assays. In addition, the MTase domain of NS5 and the C-terminal domain of p53 were mapped to be responsible for the interaction between these two proteins. We further showed that ZIKV-NS5 was colocalized with p53 and increased its protein level in the nuclei and able to prolong the half-life of p53. Furthermore, lentivirus-mediated expression of ZIKV-NS5 in hNPCs led to an apparent cell death phenotype. ZIKV-NS5 promoted the cleavage of PARP1 and significantly increased the cell apoptosis of h NPCs.Taken together, these findings revealed that ZIKV-NS5 is a previously undiscovered regulator of p53-mediated apoptosis in hNPCs, which may contribute to the ZIKV-caused abnormal neurodevelopment. | Ping Li Hualian Jiang Hong Peng Weijie Zeng Yongheng Zhong Miao He Luyang Xie Junhai Chen Deyin Guo Junyu Wu Chun-Mei Li | 2021 | Virologica Sinica2021，36，6： | 2 |
| 15 | Electron microscopy studies of the coronavirus ribonucleoprotein complex显示文摘 | Gui, Miao Liu, Xin Guo, Deyin Zhang, Zhen Yin, Chang-Cheng Chen, Yu Xiang, Ye | 2017 | Protein & Cell2017，8，3： | 2 |
| 16 | Old Weapon for New Enemy:Drug Repurposing for Treatment of Newly Emerging Viral Diseases显示文摘Emerging and re-emerging viral diseases are a public health concern for the whole world and pose a major threat to human health and life.In last decades,numerous major outbreaks of emerging and re-emerging viral diseases with gross public concern were recorded in different regions,including Ebola in western Africa,Zika in South America. | Deyin Guo | 2020 | Virologica Sinica2020，35，3： | 1 |
| 17 | Innovations and stepwise evolution of CBFs/DREB1s and their regulatory networks in angiosperms显示文摘The C-repeat binding factors/dehydrationresponsive element binding protein 1 s(CBFs/DREB1 s)have been identified as major regulators of cold acclimation in many angiosperm plants.However,their origin and evolutionary process associated to cold responsiveness are still lacking.By integrating multi-omics data of genomes,transcriptomes,and CBFs/DREB1 s genome-wide binding profiles,we unveil the origin and evolution of CBFs/DREB1 s and their regulatory network.Gene collinearity and phylogeny analyses show that CBF/DREB1 is an innovation evolved from tandem duplication-derived DREBⅢgene.A subsequent event of e-whole genome duplication led to two CBF/DREB1 archetypes(CladesⅠandⅡ)in ancient angiosperms.In contrast to cold-insensitivity of Clade I and their parent DREBⅢgenes,CladeⅡevolved a further innovation in cold-sensitive response and was stepwise expanded in eudicots and monocots by independent duplications.In geological time,the duplication events were mainly enriched around the Cretaceous-Paleogene(K-Pg)boundary and/or in the Late Cenozoic Ice Age,when the global average temperature significantly decreased.Consequently,the duplicated CBF/DREB1 genes contributed to the rewiring of CBFs/DREB1 s-regulatory network for cold tolerance.Altogether,our results highlight an origin and convergent evolution of CBFs/DREB1 s and their regulatory network probably for angiosperms adaptation to global cooling. | Yuqi Nie Liangyu Guo Fuqiang Cui Yirong Shen Xiaoxue Ye Deyin Deng Shuo Wang Jianhua Zhu Wenwu Wu | 2022 | Journal of Integrative Plant Biology2022，64，11： | 1 |
| 18 | Identification of small interfering RNAs which inhibit the replication of several Enterovirus 71 strains in China显示文摘 | Zhiqiang Wu Fan Yang Rong Zhao Lina Zhao Deyin Guo Qi Jin | 2009 | Journal of Virological Methods2009，，2： | 1 |
| 19 | The sumoylation of zinc‐fingers and homeoboxes 1 (ZHX1) by ubc9 regulates its stability and transcriptional repression activity显示文摘 | Shuliang Chen Xiao Yu Quan Lei Lixin Ma Deyin Guo | 2013 | J Cell Biochem2013，，10： | 1 |
| 20 | Severe acute respiratory syndrome coronavirus protein 6 mediates ubiquitin-dependent proteosomal degradation of N-Myc(and STAT) interactor显示文摘Severe acute respiratory syndrome coronavirus(SARS-Co V) encodes eight accessory proteins, the functions of which are not yet fully understood. SARS-Co V protein 6(P6) is one of the previously studied accessory proteins that have been documented to enhance viral replication and suppress host interferon(IFN) signaling pathways. Through yeast two-hybrid screening, we identified eight potential cellular P6-interacting proteins from a human spleen c DNA library. For further investigation, we targeted the IFN signaling pathway-mediating protein, N-Myc(and STAT) interactor(Nmi). Its interaction with P6 was confirmed within cells. The results showed that P6 can promote the ubiquitin-dependent proteosomal degradation of Nmi. This study revealed a new mechanism of SARS-Co V P6 in limiting the IFN signaling to promote SARS-Co V survival in host cells. | Weijia Cheng Shiyou Chen Ruiling Li Yu Chen Min Wang Deyin Guo | 2015 | Virologica Sinica2015，30，2： | 1 |
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