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| 1 | SARS-Coronavirus-2 Nsp13 Possesses NTPase and RNA Helicase Activities That Can Be Inhibited by Bismuth Salts显示文摘The ongoing outbreak of Coronavirus Disease 2019(COVID-19)has become a global public health emergency.SARScoronavirus-2(SARS-CoV-2),the causative pathogen of COVID-19,is a positive-sense single-stranded RNA virus belonging to the family Coronaviridae.For RNA viruses,virus-encoded RNA helicases have long been recognized to play pivotal roles during viral life cycles by facilitating the correct folding and replication of viral RNAs.Here,our studies show that SARS-CoV-2-encoded nonstructural protein 13(nsp13)possesses the nucleoside triphosphate hydrolase(NTPase)and RNA helicase activities that can hydrolyze all types of NTPs and unwind RNA helices dependently of the presence of NTP,and further characterize the biochemical characteristics of these two enzymatic activities associated with SARS-CoV-2 nsp13.Moreover,we found that some bismuth salts could effectively inhibit both the NTPase and RNA helicase activities of SARS-CoV-2 nsp13 in a dose-dependent manner.Thus,our findings demonstrate the NTPase and helicase activities of SARS-CoV-2 nsp13,which may play an important role in SARS-CoV-2 replication and serve as a target for antivirals. | Ting Shu Muhan Huang Di Wu Yujie Ren Xueyi Zhang Yang Han Jingfang Mu Ruibing Wang Yang Qiu Ding-Yu Zhang Xi Zhou | 2020 | Virologica Sinica2020，35，3： | 11 |
| 2 | The ORF3a protein of SARS-CoV-2 induces apoptosis in cells显示文摘Severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)has caused the ongoing pandemic of Coronavirus Disease 2019.SARS-CoV-2 belongs to the genus Betacoronavirus of the Coronaviridae family,which includes SARS-CoV and Middle East respiratory syndrome coronavirus.1,2 Coronavirus-encoded accessory proteins play critical roles in virus–host interactions and the modulation of host immune responses,thereby contributing to coronaviral pathogenicity via different strategies.3 However,the functions of SARS-CoV-2-encoded accessory proteins are not well understood.Apoptosis is a predominant type of programmed cell death,and has been recognized as an important host antiviral defense mechanism that controls viral infection and regulates the inflammatory response.4,5 Previous studies have reported that the SARS-CoV-encoded accessory protein ORF3a can induce apoptosis in cells,6,7 leading to the question of whether SARS-CoV-2 ORF3a also has pro-apoptotic activity.Here,we investigated the potential apoptosis-inducing activity of SARS-CoV-2 ORF3a in different cell lines and compared the pro-apoptotic activities of SARS-CoV-2 ORF3a with those of SARS-CoV ORF3a using the same system. | Yujie Ren Ting Shu Di Wu Jingfang Mu Chong Wang Muhan Huang Yang Han Xue-Yi Zhang Wei Zhou Yang Qiu Xi Zhou | 2020 | Cellular & Molecular Immunology2020，17，8： | 11 |
| 3 | Plasma metabolomic and lipidomic alterations associated with COVID-19显示文摘The pandemic of the coronavirus disease 2019(COVID-19)has become a global public health crisis.The symptoms of COVID-19 range from mild to severe,but the physiological changes associated with COVID-19 are barely understood.In this study,we performed targeted metabolomic and lipidomic analyses of plasma from a cohort of patients with COVID-19 who had experienced different symptoms.We found that metabolite and lipid alterations exhibit apparent correlation with the course of disease in these patients,indicating that the development of COVID-19 affected their whole-body metabolism.In particular,malic acid of the TCA cycle and carbamoyl phosphate of the urea cycle result in altered energy metabolism and hepatic dysfunction,respectively.It should be noted that carbamoyl phosphate is profoundly down-regulated in patients who died compared with patients with mild symptoms.And,more importantly,guanosine monophosphate(GMP),which is mediated not only by GMP synthase but also by CD39 and CD73,is significantly changed between healthy subjects and patients with COVID-19,as well as between the mild and fatal cases.In addition,dyslipidemia was observed in patients with COVID-19.Overall,the disturbed metabolic patterns have been found to align with the progress and severity of COVID-19.This work provides valuable knowledge about plasma biomarkers associated with COVID-19 and potential therapeutic targets,as well as an important resource for further studies of the pathogenesis of COVID-19. | Di Wu Ting Shu Xiaobo Yang Jian-Xin Song Mingliang Zhang Chengye Yao Wen Liu Muhan Huang Yuan Yu Qingyu Yang Tingju Zhu Jiqian Xu Jingfang Mu Yaxin Wang Hong Wang Tang Tang Yujie Ren Yongran Wu Shu-Hai Lin Yang Qiu Ding-Yu Zhang You Shang Xi Zhou | 2020 | National Science Review2020，7，7： | 9 |
| 4 | SARS-CoV-2-encoded nucleocapsid protein acts as a viral suppressor of RNA interference in cells显示文摘Dear Editor,Coronaviruses (Co Vs) are large enveloped non-segmented positive-strand RNA viruses that broadly distribute among humans and other animal species, including bats, mice and birds. SARS-Co V-2 infections can cause diseases, named the 2019 novel coronavirus disease (COVID-19). The symptoms of COVID-19 range from mild symptoms to severe respiratory syndromes, including pneumonia, and even death(Chen et al., 2020b;Jiang and Shi, 2020;Xia et al., 2020). | Jingfang Mu Jiuyue Xu Leike Zhang Ting Shu Di Wu Muhan Huang Yujie Ren Xufang Li Qing Geng Yi Xu Yang Qiu Xi Zhou | 2020 | Science China(Life Sciences)2020，63，9： | 5 |
| 5 | 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 |
| 6 | Hepatitis C Virus NS2 Protein Suppresses RNA Interference in Cells显示文摘RNAi interference(RNAi)is an evolutionarily conserved post-transcriptional gene silencing mechanism and has been well recognized as an important antiviral immunity in eukaryotes.Numerous viruses have been shown to encode viral suppressors of RNAi(VSRs)to antagonize antiviral RNAi.Hepatitis C virus(HCV)is a medically important human pathogen that causes acute and chronic hepatitis.In this study,we screened all the nonstructural proteins of HCV and found that HCV NS2 could suppress RNAi induced either by small hairpin RNAs(shRNAs)or small interfering RNAs(siRNAs)in mammalian cells.Moreover,we demonstrated that NS2 could suppress RNAi via its direct interaction with doublestranded RNAs(dsRNAs)and siRNAs,and further identified that the cysteine 184 of NS2 is required for the RNAi suppression activity through a serial of point mutation analyses.Together,our findings uncovered that HCV NS2 can act as a VSR in vitro,thereby providing novel insights into the life cycle and virus-host interactions of HCV. | Hui Zhou Qi Qian Ting Shu Jiuyue Xu Jing Kong Jingfang Mu Yang Qiu Xi Zhou | 2020 | Virologica Sinica2020，35，4： | 3 |
| 7 | The role of viral protein Ac34 in nuclear relocation of subunits of the actin-related protein 2/3 complex显示文摘The actin nucleator actin-related protein complex(Arp2/3) is composed of seven subunits: Arp2,Arp3, p40/ARPC1(P40), p34/ARPC2(P34), p21/ARPC3(P21), p20/ARPC4(P20), and p16/ARPC5(P16). Arp2/3 plays crucial roles in a variety of cellular activities through regulation of actin polymerization. Autographa californica multiple nucleopolyhedrovirus(Ac MNPV), one of the beststudied alphabaculoviruses, induces Arp2/3 nuclear relocation and mediates nuclear actin polymerization to assist in virus replication. We have demonstrated that Ac34, a viral late-gene product, induces translocation of the P40 subunit of Arp2/3 to the nucleus during Ac MNPV infection. However, it remains unknown whether Ac34 could relocate other Arp2/3 subunits to the nucleus. In this study, the effects of the viral protein Ac34 on the distribution of these subunits were studied by an immunofluorescence assay. Arp2, P34, P21, and P20 cloned from Spodoptera frugiperda(Sf9) cells showed mainly cytoplasmic localization and were relocated to the nucleus in the presence of Ac34. In addition, Arp3 was localized in the cytoplasm in both the presence and absence of Ac34, and P16 showed whole-cell localization. In contrast to Sf9 cells, all subunits of mammalian Arp2/3 showed no nuclear relocation in the presence of Ac34. Co-immunoprecipitation analysis of the interaction between Ac34 and Arp2/3 subunits revealed that Ac34 bound to P40,P34, and P20 of Sf9 cells. However, none of the subunits of mammalian Arp2/3 interacted with Ac34, indicating that protein-protein interaction is essential for Ac34 to relocate Arp2/3 subunits to the nucleus. | Jingfang Mu Yongli Zhang Yangyang Hu Xue Hu Yuan Zhou Xinwen Chen Yun Wang | 2016 | Virologica Sinica2016，31，6： | 1 |
| 8 | Reviving chloroquine for anti-SARS-CoV-2 treatment with cucurbit[7]uril-based supramolecular formulation显示文摘The wide-spreading SARS-CoV-2 virus has put the world into boiling water for more than a year,however pharmacological therapies to act effectively against coronavirus disease 2019(COVID-19)remain elusive.Chloroquine(CQ),an antimalarial drug,was found to exhibit promising antiviral activity in vitro and in vivo at a high dosage,thus CQ was approved by the FDA for the emergency use authorization(EUA)in the fight against COVID-19 in the US,but later was revoked the EUA status due to the severe clinical toxicity.Herein,we show that supramolecular formulation of CQ by a macrocyclic host,curcurbit[7]uril(CB[7]),reduced its non-specific toxicity and improved its antiviral activity against coronavirus,working in synergy with CB[7].CB[7]was found to form 1:1 host-guest complexes with CQ,with a binding constant of$104 L/mol.The CQ-CB[7]formulation decreased the cytotoxicity of CQ against Vero E6 and L-02 cell lines.In particular,the cytotoxicity of CQ(60 mmol/L)against both Vero E6 cell line and L-02 cell lines was completely inhibited in the presence of 300 mmol/L and 600 mmol/L CB[7],respectively.Furthermore,the CB[7]alone showed astonishing antiviral activity in SARS-CoV-2 infected Vero E6 cells and mouse hepatitis virus strain A59(MHV-A59)infected N2 A cells,and synergistically improved the antiviral activity of CQ-CB[7],suggesting that CB[7]-based CQ formulation has a great potential as a safe and effective antiviral agent against SARS-CoV-2 and other coronavirus. | Cheryl H.T.Kwong Jingfang Mu Shengke Li Yaohui Fang Qianyun Liu Xiangjun Zhang Hiotong Kam Simon M.Y.Lee Yu Chen Fei Deng Xi Zhou Ruibing Wang | 2021 | Chinese Chemical Letters2021，32，10： | 1 |
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