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CCS Chemistry 2024年第4期6卷 953-963页

作者： Yicong Dai Xucong Teng Difei Hu Qiushuang Zhang Jinghong Li Department of Chemistry Center for Bioanalytical ChemistryKey Laboratory of Bioorganic Phosphorus Chemistry and Chemical BiologyTsinghua UniversityBeijing 100084 New Cornerstone Science Laboratory Shenzhen 518054 Beijing Life Science Academy Beijing 102209 Center for Bioanalytical Chemistry Hefei National Laboratory of Physical Sciences at the MicroscaleUniversity of Science and Technology of ChinaHefei 230026

Genomic surveillance of monkeypox virus(MPXV)is essential to explore the reason of its unusual *** phylogenomic analysis of the MPXV genome mainly focuses on the effect of amino acid ***,we explore the evolutionary variation of RNA G-quadruplex(RG4)of MPXV and find that the genome evolution of MPXV can also produce new effects through changes in the RG4 *** RG4 is located in MPXV’s only Kelch-like C9L gene,which encodes for an antagonist of the innate immune *** evolution of this virus increases the unfolding kinetic constant of C9L RG4 and promotes the C9 protein level in living ***,all reported MPXV genomes in 2022 carry the C9L-RG4-5 pattern with the highest unfolding kinetic ***,the RG4 ligand,RGB-1,can impede the unfolding of C9L-RG4-5 and thereby reduce the C9 protein *** findings carve out a new path to comprehensively understanding MPXV virology.

关键词： G-quadruplex RNA secondary structure unfolding kinetics monkeypox virus genomic evolution immune evasion

Unveiling T cell evasion mechanisms to immune checkpoint inhibitors in acute myeloid leukemia

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Cancer Drug Resistance 2023年第3期6卷 674-687页

作者： Lindsay Gurska Kira Gritsman Department of Cell Biology Albert Einstein College of MedicineBronxNY 10461USA Department of Medical Oncology Montefiore Medical CenterAlbert Einstein College of MedicineBronxNY 10461USA

Acute myeloid leukemia (AML) is a heterogeneous and aggressive hematologic malignancy that is associated with a high relapse rate and poor prognosis. Despite advances in immunotherapies in solid tumors and other hematologic malignancies, AML has been particularly difficult to treat with immunotherapies, as their efficacy is limited by the ability of leukemic cells to evade T cell recognition. In this review, we discuss the common mechanisms of T cell evasion in AML: (1) increased expression of immune checkpoint molecules;(2) downregulation of antigen presentation molecules;(3) induction of T cell exhaustion;and (4) creation of an immunosuppressive environment through the increased frequency of regulatory T cells. We also review the clinical investigation of immune checkpoint inhibitors (ICIs) in AML. We discuss the limitations of ICIs, particularly in the context of T cell evasion mechanisms in AML, and we describe emerging strategies to overcome T cell evasion, including combination therapies. Finally, we provide an outlook on the future directions of immunotherapy research in AML, highlighting the need for a more comprehensive understanding of the complex interplay between AML cells and the immune system.

关键词： Acute myeloid leukemia T cells immune checkpoint immune evasion

Viral suppression of innate immunity via spatial isolation of TBK1/IKKε from mitochondrial antivirai platform

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Journal of Molecular Cell Biology 2014年第4期8卷 324-337页

作者： Yun-Jia Ning Manli Wang Maping Deng Shu Shen Wei Liu Wu-Chun Cao Fei Deng Yan-Yi Wang Zhihong Hu Hualin Wang State Key Laboratory of Virology Wuhan Institute of Virology Chinese Academy of Sciences Wuhan 430071 China State Key Laboratory of Pathogen and Biosecurity Beijing Institute of Microbiology and Epidemiology Beijing 100071 China

For antiviral signaling mediated by retinoic acid-inducible gene I （RiG-I）-like receptors （RLRs）, the recruitment of cytosoUc RLRs and downstream molecules （such as TBK1 and IKKε） to mitochondriaL platform is a central event that facilitates the establishment of host antiviral state. Here, we present an example of viral targeting for immune evasion through spatial isolation of TBK1/IKKε from mitochond riai antiviral platform, which was employed by severe fever with thrombocytopenia syndrome virus （SFTSV）, a deadly bunyavirus emerging recently. We showed that SFTSV nonstructural protein NSs functions as the interferon （IFN） antagonist, mainly via suppressing TBK1/IKKε-IRF3 signaling. NSs mediates the formation of cytoplasmic inclusion bodies （IBs）, and the blockage of IB formation impairs IFN-inhibiting activity of NSs. We next demonstrate that I Bs are utilized to compartmentalize TBK1/I KKε. The compartmentalization results in spatial isolation of the kinases from mitochondria, and deprived TBK1/IKKε may participate in antiviral complex assembly, leadingto the blockage of lFN ind uction. This study proposes a new role of viral I Bs as virus-built＇jail＇ for imprisoning cellular factors and presents a novel and likely common mechanism of viral immune evasion through spatial isolation of critical signaling molecules from the mitochondrial antiviral platform.

关键词： innate immunity immune evasion severe fever with thrombocytopenia syndrome virus inclusion bodies TBK1/IKKε spatial isolation

Coronavirus transmissible gastroenteritis virus antagonizes the antiviral effect of the microRNA miR-27b via the IRE1 pathway

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Science China(Life Sciences) 2022年第7期65卷 1413-1429页

作者： Changlin Wang Mei Xue Peng Wu Honglei Wang Zhongqing Liu Guangzheng Wu Pinghuang Liu Keliang Wang Wanhai Xu Li Feng Department of Urology the Fourth Affiliated Hospital of Harbin Medical UniversityHarbin 150001China State Key Laboratory of Veterinary Biotechnology Harbin Veterinary Research InstituteChinese Academy of Agricultural SciencesHarbin 150069China NHC Key Laboratory of Molecular Probes and Targeted Diagnosis and Therapy Harbin Medical UniversityHarbin 150001China

Although the functional parameters of micro RNAs(mi RNAs)have been explored to some extent,the roles of these molecules in coronavirus infection and the regulatory mechanism of mi RNAs in virus infection are still *** gastroenteritis virus(TGEV)is an enteropathgenic coronavirus and causes high morbidity and mortality in suckling ***,we demonstrated that microRNA-27b-3p(miR-27b-3p)suppressed TGEV replication by directly targeting porcine suppressor of cytokine signaling 6(SOCS6),while TGEV infection downregulated miR-27b-3p expression in swine testicular(ST)cells and in ***,the decrease of miR-27b-3p expression during TGEV infection was mediated by the activated inositolrequiring enzyme 1(IRE1)pathway of the endoplasmic reticulum(ER)*** studies showed that when ER stress was induced by TGEV,IRE1 acted as an RNase activated by autophosphorylation and unconventionally spliced m RNA encoding a potent transcription factor,X-box-binding protein 1(Xbp1s).Xbp1s inhibited the transcription of miR-27 and ultimately reduced the production of ***,our findings indicate that TGEV inhibits the expression of an anti-coronavirus micro RNA through the IRE1 pathway and suggest a novel way in which coronavirus regulates the host cell response to infection.

关键词： coronavirus transmissible gastroenteritis coronavirus(TGEV) micro RNA inositol-requiring enzyme 1(IRE1) immune evasion

The role of chemokines in acute and chronic hepatitis C infection

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Cellular & Molecular Immunology 2014年第1期11卷 25-40页

作者： Stephen Fahey Eugene Dempsey Aideen Long Institute of Molecular Medicine Trinity College Dublin Trinity Centre for Health Sciences St James's Hospital Dublin Ireland School of Biomolecular and Biomedical Science Conway Institute University College Dublin Dublin Ireland

Hepatitis C imposes a significant burden on global healthcare. Chronic infection is associated with progressive inflammation of the liver which typically manifests in cirrhosis, organ failure and cancer. By virtue of elaborate evasion strategies, hepatitis C virus （HCV） succeeds as a persistent human virus. It has an extraordinary capacity to subvert the immune response enabling it to establish chronic infections and associated liver disease. Chemokines are low molecular weight chemotactic peptides that mediate the recruitment of inflammatory cells into tissues and back into the lymphatics and peripheral blood. Thus, they are central to the temporal and spatial distribution of effector and regulatory immune cells. The interactions between chemokines and their cognate receptors help shape the immune response and therefore, have a major influence on the outcome of infection. However, chemokines represent a target for modulation by viruses including the HCV. HCV is known to modulate chemokine expression in vitro and may therefore enable its survival by subverting the immune response in vivo through altered leukocyte chemotaxis resulting in impaired viral clearance and the establishment of chronic low-grade inflammation. In this review, the roles of chemokines in acute and chronic HCV infection are described with a particular emphasis placed on chemokine modulation as a means of immune subversion. We provide an in depth discussion of the part played by chemokines in mediating hepatic fibrosis while addressing the potential applications for these chemoattractants in prognostic medicine.

关键词： chemokine chemokine receptor hepatic fibrosis hepatitis C virus immune evasion

The roles of ebolavirus glycoproteins in viral pathogenesis

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Virologica Sinica 2017年第1期32卷 3-15页

作者： Yun-Jia Ning Fei Deng Zhihong Hu Hualin Wang State Key Laboratory of Virology Wuhan Institute of Virology Chinese Academy of Sciences

Ebolaviruses are highly dangerous pathogens exhibiting extreme virulence in humans and nonhuman primates. The majority of ebolavirus species, most notably Zaire ebolavirus, can cause Ebola virus disease(EVD), formerly known as Ebola hemorrhagic fever, in humans. EVD is associated with case-fatality rates as high as 90%, and there is currently no specific treatment or licensed vaccine available against EVD. Understanding the molecular biology and pathogenesis of ebolaviruses is important for the development of antiviral therapeutics. Ebolavirus encodes several forms of glycoproteins(GPs), which have some interesting characteristics, including the transcriptional editing coding strategy and extensive O-glycosylation modification, clustered in the mucin-like domain of GP1, full-length GP(GP_(1,2)), and shed GP. In addition to the canonical role of the spike protein, GP_(1,2), in viral entry, ebolavirus GPs appear to have multiple additional functions,likely contributing to the complex pathogenesis of the virus. Here, we review the roles of ebolavirus GPs in viral pathogenesis.

关键词： ebolavirus glycoprotein (GP) mucin-like domain (MLD) cytotoxicity immune evasion inflammation pathogenesis

N^(6)-methyladenosine(m^(6)A)RNA modification in tumor immunity

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Cancer Biology & Medicine 2022年第4期19卷 385-397页

作者： Siyi Zheng Hui Han Shuibin Lin Center for Translational Medicine Precision Medicine InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Department of Otolaryngology Center for Translational MedicinePrecision Medicine InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China

Growing evidence supports that cancer progression is closely associated with the tumor microenvironment and immune ***,recent studies have revealed the crucial roles of epigenetic regulators in shaping the tumor microenvironment and restoring immune recognition.N^(6)-methyladenosine(m^(6)A)modification,the most prevalent epigenetic modification of mammalian mRNAs,has essential functions in regulating the processing and metabolism of its targeted RNAs,and therefore affects various biological processes including tumorigenesis and *** studies have demonstrated the critical functions and molecular mechanisms underlying abnormal m^(6)A modification in the regulation of tumor *** this review,we summarize recent research progress in the potential roles of m^(6)A modification in tumor immunoregulation,with a special focus on the anti-tumor processes of immune cells and involvement in immune-associated molecules and ***,we review current knowledge regarding the close correlation between m6A-related risk signatures and the tumor immune microenvironment landscape,and we discuss the prognostic value and therapeutic efficacy of m^(6)A regulators in a variety of cancer types.

关键词： N^(6)-methyladenosine(m^(6)A)modification immune evasion tumor microenvironment(TME) tumor immunology immune cells

HIV-1 Vif suppresses antiviral immunity by targeting STING

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Cellular & Molecular Immunology 2022年第1期19卷 108-121页

作者： Yu Wang Gui Qian Lingyan Zhu Zhuo Zhao Yinan Liu Wendong Han Xiaokai Zhang Yihua Zhang Tingrong Xiong Hao Zeng Xianghui Yu Xiaofang Yu Xiaoyan Zhang Jianqing Xu Quanming Zou Dapeng Yan Department of Immunology School of Basic Medical SciencesShanghai Institute of Infectious Disease and Biosecurity&Shanghai Public Health Clinical CenterFudan UniversityShanghai 200032China National Engineering Research Centre of Immunological Products Department of Microbiology and Biochemical PharmacyCollege of PharmacyArmy Medical UniversityChongqing 400038China Department of Basic Courses NCO SchoolArmy Medical UniversityShijiazhuang 050081China Biosafety Level 3 Laboratory Fudan UniversityShanghai 200032China National Engineering Laboratory for AIDS Vaccine School of Life SciencesJilin UniversityChangchun 130012China institute of Virology and AIDS Research The First Hospital of Jilin UniversityChangchun 130061China Shanghai Key Laboratory of Organ Transplantation Zhongshan Hospital&Institutes of Biomedical SciencesFudan UniversityShanghai 200032China

HIV-1 infection-induced cGAS–STING–TBK1–IRF3 signaling activates innate immunity to produce type I interferon(IFN).The HIV-1 nonstructural protein viral infectivity factor(Vif)is essential in HIV-1 replication,as it degrades the host restriction factor ***,whether and how it regulates the host immune response remains to be *** this study,we found that Vif inhibited the production of type I IFN to promote immune ***-1 infection induced the activation of the host tyrosine kinase FRK,which subsequently phosphorylated the immunoreceptor tyrosine-based inhibitory motif(ITIM)of Vif and enhanced the interaction between Vif and the cellular tyrosine phosphatase SHP-1 to inhibit type I ***,the association of Vif with SHP-1 facilitated SHP-1 recruitment to STING and inhibited the K63-linked ubiquitination of STING at Lys337 by dephosphorylating STING at ***,the FRK inhibitor D-65495 counteracted the phosphorylation of Vif to block the immune evasion of HIV-1 and antagonize *** findings reveal a previously unknown mechanism through which HIV-1 evades antiviral immunity via the ITIM-containing protein to inhibit the posttranslational modification of *** results provide a molecular basis for the development of new therapeutic strategies to treat HIV-1 infection.

关键词： Vif cGAS-STING FRK immune evasion

Foot-and-Mouth Disease Virus Inhibits RIP2 Protein Expression to Promote Viral Replication

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Virologica Sinica 2021年第4期36卷 608-622页

作者： Huisheng Liu Qiao Xue Zixiang Zhu Fan Yang Weijun Cao Xiangtao Liu Haixue Zheng State Key Laboratory of Veterinary Etiological Biology National Foot and Mouth Diseases Reference LaboratoryKey Laboratory of Animal Virology of Ministry of AgricultureLanzhou Veterinary Research InstituteChinese Academy of Agricultural SciencesLanzhou 730046China

Receptors interaction protein 2(RIP2)is a specific adaptor molecule in the downstream of *** role of RIP2 during foot-and-mouth disease virus(FMDV)infection remains ***,our results showed that RIP2 inhibited FMDV replication and played an important role in the activation of IFN-βand NF-κB signal pathways during FMDV *** infection triggered RIP2 transcription,while it reduced the expression of RIP2 *** analysis showed that FMDV 2B,2C,3C^(pro),and L^(pro) proteins were responsible for inducing the reduction of RIP2 protein.3C^(pro) and L^(pro) are viral proteinases that can induce the cleavage or reduction of many host proteins and block host protein *** carboxyl terminal 105-C114 and 135-C144 regions of 2B were essential for reduction of *** results also showed that the N terminal 1-61 region of 2C were essential for the reduction of *** 2C-induced reduction of RIP2 was dependent on inducing the reduction of poly(A)-binding protein 1(PABPC1).The interaction between RIP2 and 2C was observed in the context of viral infection,and the residues 1-61 were required for the *** data clarify novel mechanisms of reduction of RIP2 mediated by FMDV.

关键词： Foot-and-mouth disease virus(FMDV) Receptors interaction protein 2(RIP2) PABPC1 2C immune evasion

Inducible Rubicon facilitates viral replication by antagonizing interferon production

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Cellular & Molecular Immunology 2017年第7期14卷 607-620页

作者： Yushun Wan Wei Cao Tao Han Sheng Ren Jian Feng TieLong Chen Jun Wang Ruth Broering Mengji Lu Ying Zhu State Key Laboratory of Virology and College of Life Sciences Wuhan UniversityWuhan 430072China Department of Infectious Diseases Zhongnan Hospital of Wuhan UniversityWuhan 430072China Medical Faculty Department of Gastroenterology and HepatologyUniversity of Duisburg-EssenEssen 45127Germany Institute of Virology University of Duisburg-EssenEssen 45127Germany

The RUN domain Beclin-1-interacting cysteine-rich-containing(Rubicon)protein is involved in the maturation step of autophagy and the endocytic pathway as a Beclin-1-binding partner,but little is known regarding the role of Rubicon during viral ***,we performed functional studies of the identified target in interferon(IFN)signaling pathways associated with Rubicon to elucidate the mechanisms of viral resistance to *** Rubicon protein levels were elevated in peripheral blood mononuclear cells,sera and liver tissues from patients with hepatitis B virus(HBV)infection relative to those in healthy *** of the overexpression and knockdown of Rubicon showed that Rubicon significantly promoted HBV *** addition,Rubicon knockdown resulted in the inhibition of enterovirus 71,influenza A virus and vesicular stomatitis *** expression o0f Rubicon led to the suppression of virus-induced type-I interferon(IFN-αand IFN-β)and type-III interferon(IFN-λ1).Translocation of activated IRF3 and IRF7 from the cytoplasm to the nucleus was involved in this process,and the NF-κB essential modulator(NEMO),a key factor in the IFN pathway,was the target with which Rubicon *** results reveal a previously unrecognized function of Rubicon as a virus-induced protein that binds to NEMO,leading to the inhibition of type-I interferon *** thus functions as an important negative regulator of the innate immune response,enhances viral replication and may play a role in viral immune evasion.

关键词： host response immune evasion interferon Rubicon viral infection