Seminars in virology最新文献

{"title":"Apoptosis in Alphavirus Encephalitis","authors":"Diane E. Griffin,&nbsp;J.Marie Hardwick","doi":"10.1006/smvy.1998.0152","DOIUrl":"10.1006/smvy.1998.0152","url":null,"abstract":"<div><p>Sindbis virus causes acute encephalitis in mice and serves as a useful model for encephalitic alphaviruses that infect humans. The outcome of infection is determined by whether infected neurons are resistant to virus-induced programmed cell death or activate their apoptotic pathway. The host immune response may also cause death of infected neurons. Determinants of neuronal apoptosis include the maturity of the neuron, the virulence of the infecting virus and the cellular immune response to infection. In many situations viral and cellular factors that decrease virus replication also decrease apoptosis. Antiviral antibody can downregulate virus replication in surviving neurons without affecting cell viability. Other innate and induced host immune responses can alter the outcome of infection without a change in virus production. Failure to induce apoptosis in infected neurons leads to long-term persistence of small amounts of viral RNA in the nervous system of infected mice despite the clearance of infectious virus. The molecular mechanisms that govern these pathogenesis factors are beginning to be elucidated.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 6","pages":"Pages 481-489"},"PeriodicalIF":0.0,"publicationDate":"1998-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1998.0152","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of Apoptosis by Poxviruses","authors":"Peter C. Turner,&nbsp;Richard W. Moyer","doi":"10.1006/smvy.1998.0150","DOIUrl":"10.1006/smvy.1998.0150","url":null,"abstract":"<div><p>Poxviruses express a variety of proteins which can function to inhibit apoptosis in infected cells, allowing virus replication to continue and conferring a broad host range. Some poxvirus antiapoptosis proteins act by sequestering or inactivating inducers of apoptosis such as dsRNA and superoxide anions. Others interfere with signaling by receptors including those belonging to the TNF receptor superfamily that would otherwise activate a proteolytic cascade that terminates with the cleavage of death substrates. The cowpox virus crmA protein directly inhibits cysteine proteinases within the cascade and can also block apoptosis triggered by the serine proteinase granzyme B. Finally there are poxvirus antiapoptosis proteins containing ankyrin repeat regions that are thought to interact with cellular proteins.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 6","pages":"Pages 453-469"},"PeriodicalIF":0.0,"publicationDate":"1998-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1998.0150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Adenoviruses: Evading Detection by Cytotoxic T Lymphocytes","authors":"G.Eric Blair ,&nbsp;Kersten T. Hall","doi":"10.1006/smvy.1997.0140","DOIUrl":"10.1006/smvy.1997.0140","url":null,"abstract":"<div><p>Human adenoviruses cause lytic and persistent respiratory, enteric, and other infections. Adenoviruses can transform primary rodent cells and certain serotypes of human adenoviruses (such as adenovirus type 12 from subgenus A) induce tumors in newborn rodents. In both cases, adenovirus gene products mediate evasion of the cellular immune system by infected and tumor cells. In viral infection, a product of the early region<em>E3</em>gene, a glycoprotein termed E3-19K, binds to and retains newly synthesised major histocompatibility complex (MHC) class I molecules in the endoplasmic reticulum thus rendering infected cells resistant to lysis by cytotoxic T lymphocytes. In addition, other products of the<em>E3</em>region confer on infected cells resistance to tumor necrosis factor-α-mediated lysis. Not all human adenovirus serotypes encode an E3-19K protein: viruses from subgenus A (such as adenovirus 12) and F (the enteric adenoviruses 40 and 41) do not encode an E3-19K molecule. In the case of Ad12, products of the viral E1A gene repress MHC class I heavy chain gene transcription. This leads to loss of MHC class I molecules from the surface of adenovirus 12-transformed cells and contributes to their evasion from cytotoxic T lymphocytes. Considerable progress has been made toward identifying the targets for E1A-mediated repression of the class I heavy chain promoter. In addition, adenovirus 12 mediates transcriptional repression of other genes in the MHC complex involved in antigen presentation, namely the transporter associated with antigen presentation (TAP) genes and MHC-encoded proteasome components, the low molecular weight proteins termed LMPs. Overall, adenoviruses display a variety of differing mechanisms for posttranslational (E3-19K) and transcriptional (E1A) repression of MHC class I expression that operate in all human viral serotypes studied, suggesting that evasion of cytotoxic T cell lysis forms an important part of the infection and oncogenic transformation strategies adopted by human adenoviruses.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 387-397"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human and Murine Cytomegalovirus Evasion of Cytotoxic T Lymphocyte and Natural Killer Cell-Mediated Immune Responses","authors":"Nicholas J. Davis-Poynter ,&nbsp;Helen E. Farrell","doi":"10.1006/smvy.1997.0142","DOIUrl":"10.1006/smvy.1997.0142","url":null,"abstract":"<div><p>Herpesviruses, such as human and murine cytomegalovirus, possess an impressive array of genes believed to assist in virus survival against the host immune response. In this review, we cover the rapidly growing area of cytomegalovirus evasion of cellular immunity, specifically cytotoxic T lymphocytes and natural killer cells. The proposed mechanisms of action of viral proteins involved in blocking peptide presentation to CD8⁺T cells, namely, interference with peptide generation, inhibition of peptide assembly with class I MHC and retention/destabilization of class I MHC complexes, are described. In addition, recent evidence implicating the viral class I MHC-like proteins as inhibitors of natural killer cell-mediated clearance is reviewed.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 369-376"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0142","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Avoiding Immunity and Apoptosis: Manipulation of the Host Environment by Herpes Simplex Virus and Epstein-Barr Virus","authors":"Ann B. Hill ,&nbsp;Maria G. Masucci","doi":"10.1006/smvy.1997.0144","DOIUrl":"10.1006/smvy.1997.0144","url":null,"abstract":"<div><p>Herpesviruses infect their hosts in early life to establish latent or persistent infection with little damage to the host. They are able to reactivate throughout the life of the host and replicate to produce an infective innoculum in the face of a fully primed immune system. They achieve this lifestyle by careful manipulation of the host environment. Here we review two aspects of host defense—apoptosis of infected cells and cytotoxic T cell recognition of infected cells. We discuss avoidance of these host responses by an α-herpesvirus, herpes simplex virus, and a γ-herpesvirus, Epstein-Barr virus.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 361-368"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0144","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51141904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abduction of Chemokine Elements by Herpesviruses","authors":"Daniel J. Dairaghi ,&nbsp;David R. Greaves ,&nbsp;Thomas J. Schall","doi":"10.1006/smvy.1997.0146","DOIUrl":"10.1006/smvy.1997.0146","url":null,"abstract":"<div><p>Chemokines play a key role in orchestrating leukocytic recruitment during inflammatory responses, including those to viral infections. Chemokines are soluble cytokines which mediate their effects through specific G protein-coupled, seven-transmembrane receptors which are expressed on a wide range of cells, including monocytes, T-cells, dendritic cells, and NK cells. Analyses of herpesvirus genomes have revealed that these viral pathogens encode their own versions of both chemokines and chemokine receptors. Viral genes encoding chemokine elements were likely to have been acquired from the host genome and have been remodeled during virus evolution to presumably optimize function or acquire new properties not displayed by their cellular homologues. Virus-encoded chemokines and chemokine receptors are important players in the continuing confrontation between viruses and their mammalian hosts. Detailed characterization of these elements will provide a better understanding of how the immune system responds to viral infection and may suggest new antiviral drug targets and new avenues for the development of antiviral therapies. We will review here the chemokine elements encoded by herpesviruses and how they may aid viral infection and propagation.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 377-385"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0146","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How Poxviruses Oppose Apoptosis","authors":"Grant McFadden ,&nbsp;Michele Barry","doi":"10.1006/smvy.1997.0141","DOIUrl":"10.1006/smvy.1997.0141","url":null,"abstract":"<div><p>Poxviruses express a variety of proteins that are able to modulate the innate cellular apoptotic response triggered by virus infection. Poxviruses are the only DNA viruses to replicate exclusively in the cytoplasm of infected cells, and to date, members of this family have been shown to encode a wide variety of proteins that block or delay apoptosis, including caspase inhibitors, other serpins, death domain effectors, bcl-2/CED-9 homologs, modulators of the FAS/TNF pathway, and inhibitors of PKR. It is predicted that this list of poxvirus apoptosis modulators will continue to grow in the coming years and should provide an increasingly rich and diverse family of apoptosis regulators.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 429-442"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poxviruses: Capturing Cytokines and Chemokines","authors":"Antonio Alcamı́ ,&nbsp;Julian A. Symons,&nbsp;Anu Khanna,&nbsp;Geoffrey L. Smith","doi":"10.1006/smvy.1997.0143","DOIUrl":"10.1006/smvy.1997.0143","url":null,"abstract":"<div><p>Cytokines play a critical role in the regulation of immune responses and constitute important targets for virus immune evasion mechanisms. One strategy used by large DNA viruses is to encode proteins that mimic cytokines or cytokine receptors, which modulate the activity of cytokines during infection. Poxviruses encode a unique set of proteins that are secreted from the infected cell and function as soluble cytokine receptors or binding proteins and sequester tumor necrosis factor, interleukin-1β, or chemokines. Characterization of these poxvirus proteins is providing information on virus pathogenesis, the function of cytokines, and new strategies for immune modulation and therapeutic intervention.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 419-427"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0143","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51141899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of Apoptosis by Human Adenovirus Genes","authors":"G. Chinnadurai","doi":"10.1006/smvy.1997.0139","DOIUrl":"10.1006/smvy.1997.0139","url":null,"abstract":"<div><p>Adenovirus infection induces apoptosis by multiple paradigms that involve viral proteins coded by three different early gene regions,<em>E1A, E3,</em>and<em>E4.</em>These cell death programs are antagonized by a different set of viral proteins coded by early gene blocks<em>E1B, E3,</em>and<em>E4.</em>The E1A proteins activate the cellular transcription factor E2F and also increase accumulation of the p53 tumor suppressor protein, both proteins with known apoptotic activity. The E1B-19K protein, a distantly related member of the BCL-2 family of antiapoptosis proteins, efficiently suppresses both p53-dependent and -independent apoptosis induced during adenovirus infection. Two other proteins, E1B-55K and E4-36K, which inactivate p53 by physical protein complex formation suppress p53-dependent apoptosis. The mechanisms by which the E1B-19K protein acts are not fully known, but at least one appears to involve antagonizing the activity of various cellular pro-apoptotic proteins such as BAX, BAK, and BIK. One of the two major E1A proteins, 289R, also appears to induce cell death via transactivation of the cellular transcription factor NF-κB as well as two early gene blocks,<em>E3</em>and<em>E4.</em>NF-κB is believed to induce expression of TNF and various inflammatory cytokines in virus-infected cells. The<em>E3</em>and<em>E4</em>gene blocks each code for a cell death protein, E3-11.6K (ADP) and E4-orf4. The E1A proteins also sensitize infected cells for TNF-induced apoptosis and this activity is linked to the cell cycle regulatory activities of E1A. In addition to the E1B-19K protein, three E3 proteins, 14.7K, 10.4K, and 14.5K, specifically protect cells against TNF-induced cell death. One of the mechanisms by which the E3-14.7K and E3-10.4K/14.5K complex suppress TNF-induced toxicity appears to be mediated by the release of arachidonic acid by the cytosolic phospholipase A2. The E3 proteins also inhibit Fas-agonist-induced apoptosis by endosome-mediated internalization and degradation of Fas from the cell surface. Suppression of E1A-induced apoptosis in nonpermissive cells by E1B-19K, E1B-55K, and E4-36K proteins leads to oncogenic transformation.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 399-408"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51142292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poxviruses: Interfering with Interferon","authors":"Geoffrey L. Smith ,&nbsp;Julian A. Symons,&nbsp;Antonio Alcamı́","doi":"10.1006/smvy.1997.0145","DOIUrl":"10.1006/smvy.1997.0145","url":null,"abstract":"<div><p>Interferon (IFN) is an important innate defense against virus infection and many viruses have consequently evolved ways to interfere with the action of IFN. The poxviruses are an excellent example and devote at least four proteins to this task. Two function within the infected cell to block the action of IFN-induced antiviral proteins, and two are secreted to capture type I and type II IFNs before they can bind to cellular IFN receptors. The vaccinia virus IFN receptors have a surprisingly broad species specificity that may aid virus replication in several species and provide clues about the enigmatic origin of vaccinia virus.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"8 5","pages":"Pages 409-418"},"PeriodicalIF":0.0,"publicationDate":"1998-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1997.0145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51141913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}