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Ebola virus VP35 perturbs type I interferon signaling to facilitate viral replication

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Virologica Sinica 2023年第6期38卷 922-930页

作者： Zengguo Cao Chenchen Liu Cheng Peng Yong Ran Yulin Yao Gengfu Xiao Entao Li Zixi Chen Xia Chuai Sandra Chiu Key Laboratory of Special Pathogens and Biosafety Wuhan Institute of VirologyCenter for Biosafety Mega-ScienceChinese Academy of SciencesWuhan430071China University of Chinese Academy of Sciences Beijing100190China National Biosafety Laboratory Chinese Academy of SciencesWuhan430020China Division of Life Sciences and Medicine University of Science and Technology of Chin1Hefei230026China Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science Shenzhen Engineering Laboratory for Marine Algal BiotechnologyGuangdong Provincial Key Laboratory for Plant EpigeneticsCollege of Life Sciences and OceanographyShenzhen UniversityShenzhen 518060China

As one of the deadliest viruses,Ebola virus(EBOV)causes lethal hemorrhagic fevers in humans and nonhuman *** suppression of innate immunity leads to robust systemic virus replication of EBOV,leading to enhanced ***,the mechanism of EBOV-host interaction is not fully ***,we identified multiple dysregulated genes in early stage of EBOV infection through transcriptomic analysis,which are highly clustered to Jak-STAT *** VP35 and VP30 were found to inhibit type I interferon(IFN)***,exogenous expression of VP35 blocks the phosphorylation of endogenous STAT1,and suppresses nuclear translocation of *** serial truncated mutations of VP35,N-terminal 1–220amino acid residues of VP35 were identified to be essential for blocking on type I IFN ***,VP35 of EBOV suppresses type I IFN signaling more efficiently than those of Bundibugyo virus(BDBV)and Marburg virus(MARV),resulting in stable replication to facilitate the ***,this study enriches understanding on EBOV evasion of innate immune response,and provides insights into the interplay between filoviruses and host.

关键词： Ebola virus(EBOV) Type I interferon(IFN)signaling viral replication

Naturally occurring PA^(E206K)point mutation in 2009 H1N1 pandemic influenza viruses impairs viral replication at high temperatures

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Virologica Sinica 2024年第1期39卷 71-80页

作者： Mengmeng Cao Qiannan Jia Jinghua Li Lili Zhao Li zhu Yufan Zhang Shan Li Tao Deng National Institute of Pathogen Biology Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing100730China CAS Key Laboratory of Pathogen Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing100101China

The emergence of influenza virus A pandemic H1N1 in April 2009 marked the first pandemic of the 21st *** this study,we observed significant differences in the polymerase activities of two clinical 2009 H1N1 influenza A virus isolates from Chinese and Japanese *** comparison of the three main protein subunits(PB2,PB1,and PA)of the viral RNA-dependent RNA polymerase complex and subsequent mutational analysis revealed that a single amino acid substitution(E206K)was responsible for the observed impaired replication *** in vitro experiments showed that presence of PAE206K decreased the replication of influenza A/WSN/33 virus in mammalian cells and a reduction in the virus’s pathogenicity in *** studies revealed that PAE206K is a temperature-sensitive mutant associated with the inability to transport PB1–PA complex to the nucleus at high temperature(39.5℃).Hence,this naturally occurring variant in the PA protein represents an ideal candidate mutation for the development of live attenuated influenza vaccines.

关键词： H1N1 Influenza A virus Polymerase acidic protein Point mutation viral replication

Melanization induced by Heliothis virescens ascovirus 3h promotes viral replication

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Insect Science 2021年第2期28卷 472-484页

作者： Zi-Qi Li Xiao-Hui Song Min Wang Shu Wang Guo-Hua Huang Hunan Provincial Key Laboratory for Biology and Control of Plant Diseases and Insect Pests Hunan Agricultural UniversityChangshaChina College of Plant Protection Hunan Agricultural UniversityChangshaChina

Melanization is an important innate immune defense mechanism of insects,which can kill invading *** pathogens,for their survival and reproduction,inhibit the melanization of the ***,our results suggested that after infection with Heliothis virescens ascovirus 3h(HvAV-3h),the speed of melanization in infected Spodoptera exigiia larval hemolymph was accelerated and that the phenoloxidase(PO)activity of hemolymph in larvae infected with HvAV-3h increased significantly(1.20-fold at 96 hpi,1.52-fold at 120 hpi,1.23-fold at 144 hpi,1.12-fold at 168 hpi).The transcription level of the gene encoding *** prophenoloxidase-1(SePPO-1 gene)was upregulated dramatically in the fat body during the middle stage of *** addition,when melanization was inhibited or promoted,the replication of HvAV-3h was inhibited or promoted,*** conclusion,infection with HvAV-3h can markedly induce melanization in the middle stage of infection,and melanization is helpful for HvAV-3h viral replication.

关键词： Heliothis virescens ascovirus 3h melanization Spodoptera exigua viral replication

Frequency of viral replication Markers in Chronic HBV Carriers in N’Djamena, Chad

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Open Journal of Gastroenterology 2022年第10期12卷 271-277页

作者： Ali Mahamat Moussa Mayanna Habkreo Adawaye Chatté Borde Emmanuel Adoum Abdelrazack Fouda Bessimbaye Nadlaou Service de Médecine Interne et Gastroentérologie CHU La Référence Nationale de N’Djamena N’Djamena Tchad Département des Sciences Biomédicales et Pharmaceutiques Faculté des Sciences de la Santé Humaine Université de N’Djamena N’Djamena Tchad Programme National de Lutte Contre le VIH/IST/Hépatite Ministère de la Santé Publique N’Djamena Tchad

Introduction: According to the WHO, Chad is located in an area of high endemicity for hepatitis B virus (HBV). The aim of this study was to analyze the virological profiles of chronic HBV carriers. Materials and Method: This was a retrospective and analytical study including outpatients with chronic HBV of any age received in Department of Internal Medicine and Gastroenterology of National General Reference Hospital of N’Djamena from 2013 to 2017. Results: During the study period, 401 chronic hepatitis B virus carriers (mean age was 35 years ± 11 years with sex ratio of 3.26) were seen in outpatient clinic with a frequency of 3.34% (401/11,988). HBeAg (+) patients were 12.8% and HBeAg negative 87.2%. HBeAg-negative patients were significantly older (p = 0.000) than those with HBeAg (+). The mean HBV-DNA level was higher in HBeAg (+) patients. The HBV-DNA level in HBeAg-positive patients was higher than in HBeAg-negative patients with a significant difference (p = 0.043). The mean ALT level was 45 IU/L in HBeAg (−) patients. It was 49 in HBeAg (+) patients. Conclusion: HBeAg (−) chronic hepatitis B is the most predominant form in our study. This observation is important because it can help to adapt the management strategies.

关键词： Chronic Hepatitis B Epidemiology HBeAg viral replication Ndjamena Chad

RIG-1 and MDA-5 signaling pathways contribute to IFN-β production and viral replication in Porcine circovirus virus type 2 infection cells

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RIG-1 and MDA-5 signaling pathways contribute to IFN-β prod...

Corilagin inhibits SARS-CoV-2 replication by targeting viral RNA-dependent RNA polymerase

中国兽医病理学2017年学术研讨会暨兽医病理学分会第九次全国会员代表大会

作者： Bei Huang Jiansheng Li Xinchen Zhang Qiling Zhao Mingqing Lu Yingjun Lv College of veterinary science Nanjing agricultural university

Interferon(IFN) is known for its antiviral ***,it is surprising that treatment of IFN-α and IFN-β in vitro enhanced replication of porcine circovirus type 2(PCV2),indicating that complex relationship between interferon and *** now,it is unclear how the interferon is produced during PCV2 infection and also not knowing whether the interferon induced by PCV2 itself can promote the viral *** the study,PCV2 induced up-regulation of IFN-β in PK-15 cell,and treatment of PCV2-infected cell with NF-κB inhibitor BAY11-7082 decreased the expression of INF-β,while treatment with IRF3 inhibitor BX795 do not,indicating that PCV2 can induce IFN-β production and the induction of IFN-β via IRF3 rather than NF-κB mediated signal ***,PCV2 increased the protein expressions of IRF3,p-IRF3,MAVS,RIG-1 and MDA-5,and knockdown of RIG-1 and MDA-5 decreased the level of IFN-β.These results demonstrate that PCV2 induces the IFN-β production by RIG-1/MDA-5/MAVS/IRFs signal ***,the viral load of PCV2 and PCV2 infection decreased after knockdown of RIG-1 and MDA-5,indicating that RIG-1 and MDA-5 signal pathway contribute to the viral *** conclusion,PCV2 induces the production of IFN-β by RIG-1 and MDA-5 signaling pathway,and the IFN-β produced during PCV2 infection facilitate the viral replication.

关键词： PCV2 Interferon viral replication RIG-1 MDA-5

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Acta Pharmaceutica Sinica B 2021年第6期11卷 1555-1567页

作者： Quanjie Li Dongrong Yi Xiaobo Lei Jianyuan Zhao Yongxin Zhang Xiangling Cui Xia Xiao Tao Jiao Xiaojing Dong Xuesen Zhao Hui Zeng Chen Liang Lili Ren Fei Guo Xiaoyu Li Jianwei Wang Shan Cen Institute of Medicinal Biotechnology Chinese Academy of Medical Sciences and Peking Union Medical SchoolBeijing 100050China Institute of Pathogen Biology Chinese Academy of Medical Sciences and Peking Union Medical SchoolBeijing 100730China Institute of Infectious Disease Beijing Ditan HospitalCapital Medical UniversityBeijing 100015China Lady Davis Institute Jewish General HospitalMc Gill UniversityMontrealQuebec H3T 1E2Canada CAMS Key Laboratory of Antiviral Drug Research Peking Union Medical CollegeChinese Academy of Medical SciencesBeijing 100730China

Severe acute respiratory syndrome coronavirus-2(SARS-CoV-2) has become one major threat to human population *** RNA-dependent RNA polymerase(RdRp) presents an ideal target of antivirals,whereas nucleoside analogs inhibitor is hindered by the proofreading activity of ***,we report that corilagin(RAI-S-37) as a non-nucleoside inhibitor of SARS-CoV-2 RdRp,binds directly to RdRp,effectively inhibits the polymerase activity in both cell-free and cell-based assays,fully resists the proofreading activity and potently inhibits SARS-CoV-2 infection with a low 50% effective concentration(EC50) value of 0.13 μmol/*** modeling predicts that RAI-S-37 lands at the palm domain of RdRp and prevents conformational changes required for nucleotide incorporation by *** addition,combination of RAI-S-37 with remdesivir exhibits additive activity against antiSARS-CoV-2 *** with the current data available on the safety and pharmacokinetics of corilagin as a medicinal herbal agent,these results demonstrate the potential of being developed into one of the much-needed SARS-CoV-2 therapeutics.

关键词： SARS-CoV-2 RdRp Structure-based virtual screening viral replication Non-nucleoside inhibitor Drug combinations Corilagin

In vitro inhibition of HIV-1 replication in autologous CD4*T cells indicates viral containment by multifactorial mechanisms

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Virologica Sinica 2017年第6期32卷 485-494页

作者： Ting Tu Jianbo Zhan Danlei Mou Wei Li Bin Su Tong Zhang Tao Li Ning Li Hao Wu Cong Jin Huabiao Chen Jiangsu Key Laboratory of Clinical Laboratory Medicine Jiangsu University School of MedicineZhenjiang 212013China National HIV/HCV Reference Laboratory National Center for AIDS/STD Control and Prevention Chinese Center for Disease Control and PreventionBeijing 102206China Hubei Provincial Center for Disease Control and Prevention Wuhan 430079China Beijing You'an Hospital Capital Medical UniversityBeijing 100069China

HIV-1-specific cytotoxic T lymphocytes(CTLs) and neutralizing antibodies(NAbs) are present during chronic infection, but the relative contributions of these effector mechanisms to viral containment remain unclear. Here, using an in vitro model involving autologous CD4+ T cells,primary HIV-1 isolates, HIV-1-specific CTLs, and neutralizing monoclonal antibodies, we show that b12, a potent and broadly neutralizing monoclonal antibody to HIV-1, was able to block viral infection when preincubated with virus prior to infection, but was much less effective than CTLs at limiting virus replication when added to infected cell cultures. However, the same neutralizing antibody was able to contain viruses by antibody-dependent cell-mediated virus inhibition in vitro,which was mediated by natural killer cells(NKs) and dependent on an Fc-Fc receptor ***, bulk CTLs from HIV-1 controllers were more effective in suppression of virus replication than those from progressors. These findings indicate that control of HIV-1 replication in activated CD4^+ T cells is ineffectively mediated by neutralizing antibodies alone, but that both CTLs and antibody-dependent NK-mediated immune mechanisms contribute to viral containment. Our study systemically compared three major players in controlling HIV-1 infection, CTLs, NAbs, and NKs, in an autologous system and highlighted the multifactorial mechanisms for viral containment and vaccine success.

关键词： HIV-1 infection viral replication cytotoxic T lymphocyte(CTL) natural killer cells neutralizing antibody

Ciclopirox inhibits SARS-CoV-2 replication by promoting the degradation of the nucleocapsid protein

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Acta Pharmaceutica Sinica B 2024年第6期14卷 2505-2519页

作者： Xiafei Wei Yuzheng Zhou Xiaotong Shen Lujie Fan Donglan Liu Xiang Gao Jian Zhou Yezi Wu Yunfei Li Wei Feng Zheng Zhang Institute for Hepatology National Clinical Research Center for Infectious DiseaseShenzhen Third People's HospitalSouthern University of Science and TechnologyShenzhen 518112China Guangzhou Laboratory Guangzhou Medical UniversityGuangzhou 511495China State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory DiseaseGuangzhou Institute of Respiratory Healththe First Affiliated Hospital of Guangzhou Medical UniversityGuangzhou 510120China

The nucleocapsid protein(NP)plays a crucial role in SARS-CoV-2 replication and is the most abundant structural protein with a long *** its vital role in severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)assembly and host inflammatory response,it remains an unexplored target for drug *** this study,we identified a small-molecule compound(ciclopirox)that promotes NP degradation using an FDA-approved library and a drug-screening cell *** significantly inhibited SARS-CoV-2 replication both in vitro and in vivo by inducing NP *** induced abnormal NP aggregation through indirect interaction,leading to the formation of condensates with higher viscosity and lower *** condensates were subsequently degraded via the autophagy-lysosomal pathway,ultimately resulting in a shortened NP half-life and reduced NP *** results suggest that NP is a potential drug target,and that ciclopirox holds substantial promise for further development to combat SARS-CoV-2 replication.

关键词： SARS-CoV-2 Nucleocapsid protein viral replication Ciclopirox Abnormal aggregation Protein degradation Autophagy-lysosome Drug target

LncRNA NKILA inhibits HBV replication by repressing NF-κB signalling activation

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Virologica Sinica 2024年第1期39卷 44-55页

作者： Xi Zhang Yuanyuan Li Chen Huan Yubao Hou Rujia Liu Hongyun Shi Peng Zhang Baisong Zheng Yingchao Wang Hong Wang Wenyan Zhang Institute of Virology and AIDS Research The First Hospital of Jilin UniversityChangchun130012China Department of Ophthalmology The First Hospital of Jilin UniversityChangchun130012China Hepatobiliary Pancreatic Surgery The First Hospital of Jilin UniversityChangchun130012China

Hepatitis B virus(HBV)infection results in liver cirrhosis and hepatocellular carcinoma(HCC).HBx/nuclear factor(NF)-κB pathway plays a role in HBV ***,whether NF-κB-interacting long noncoding RNA(NKILA),a suppressor of NF-κB activation,regulates HBV replication remains largely *** this study,gain-and-loss experiments showed that NKILA inhibited HBV replication by inhibiting NF-κB *** turn,HBV infection down-regulated NKILA *** addition,expression levels of NKILA were lower in the peripheral blood-derived monocytes(PBMCs)of HBV-positive patients than in healthy individuals,which were correlated with HBV viral *** a negative correlation between NKILA expression level and HBV viral loads was observed in blood serum from HBV-positive *** levels of endogenous NKILA were also observed in HepG2 cells expressing a 1.3-fold HBV genome,HBV-infected HepG2-NTCP cells,stable HBV-producing HepG2.2.15 and HepAD38 cells,compared to those HBV-negative ***,HBx was required for NKILA-mediated inhibition on HBV *** decreased HBx-induced NF-κB activation by interrupting the interaction between HBx and p65,whereas NKILA mutants lack of essential domains for NF-κB inhibition,lost the ability to inhibit HBV ***,our data demonstrate that NKILA may serve as a suppressor of HBV replication via NF-κB signalling.

关键词： LncRNA NF-κB-interacting longnoncoding RNA(NKILA) NF-ĸB signalling ChronichepatitisBvirus(HBV) viral replication HBx