Seminars in virology最新文献_第10页

Antiviral immunity in HIV-1 infected long-term non-progressors (LTNPs) HIV-1感染长期非进展者(ltnp)的抗病毒免疫

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0017

Giuseppe Pantaleo, Mauro Vaccarezza, Cecilia Graziosi, Oren J. Cohen, Anthony S. Fauci

{"title":"Antiviral immunity in HIV-1 infected long-term non-progressors (LTNPs)","authors":"Giuseppe Pantaleo, Mauro Vaccarezza, Cecilia Graziosi, Oren J. Cohen, Anthony S. Fauci","doi":"10.1006/smvy.1996.0017","DOIUrl":"10.1006/smvy.1996.0017","url":null,"abstract":"<div><p>Now that the acquired immunodeficiency syndrome (AIDS) epidemic is well into its second decade, it has become evident that a small percentage (approximately 5%) of HIV-infected individuals do not experience progression of HIV disease even after several years of being infected with HIV. These individuals have been designated as ‘long term non-progressors’ (LTNP). From a virologic standpoint, these LTNP have low viral burden in mononuclear cells, but persistent virus replication as manifested by chronic and generally low levels of plasma viremia. From an immunologic standpoint, immune functions including CD8<sup>+</sup>T-cell- and CD4<sup>+</sup>T-cell-mediated functions are preserved. In addition, they show a vigorous humoral immune response. More importantly, lymphoid tissue structure and function are preserved in LTNP. Despite persistent low-level virus replication and chronic stimulation of the immune system, immune activation is qualitatively and quantitatively different in LTNP compared to that observed in HIV-infected individuals whose HIV disease has progressed.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 2","pages":"Pages 131-138"},"PeriodicalIF":0.0,"publicationDate":"1996-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51136604","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}

引用次数: 7

Mechanisms of CTL-mediated cytoxicity ctl介导的细胞毒性机制

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0014

William R. Clark, Craig M. Walsh, Mehrdad Matloubian, Alison A. Glass, Fumitaka Hayashi

引用次数: 1

Cellular immunity against human papillomavirus associated cervical cancer 人乳头瘤病毒相关子宫颈癌的细胞免疫

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0015

Martin Kast W. , Mariet C.W. Feltkamp , Maaike E. Ressing , Michel P.M. Vierboom , Remco M.P. Brandt , Cornelis J.M. Melief

引用次数: 30

Introduction: Immunity to viruses 简介:对病毒免疫

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0011

Rafi Ahmed

引用次数: 0

Live attenuated HIV as a vaccine for AIDS: pros and cons 作为艾滋病疫苗的减毒活HIV:利弊

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0019

Ruth M. Ruprecht , Timothy W. Baba , An Li , Seyoum Ayehunie , Yuwen Hu , Vladimir Liska , Robert Rasmussen , Prem L. Sharma

引用次数: 12

Immunological features of murine gammaherpesvirus infection 小鼠γ疱疹病毒感染的免疫学特征

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0016

Anthony A. Nash, Edward J. Usherwood, James P. Stewart

{"title":"Immunological features of murine gammaherpesvirus infection","authors":"Anthony A. Nash, Edward J. Usherwood, James P. Stewart","doi":"10.1006/smvy.1996.0016","DOIUrl":"10.1006/smvy.1996.0016","url":null,"abstract":"<div><p>Murine gammaherpesvirus (MHV-68) represents a unique opportunity to explore the detailed interaction of a gammaherpesvirus with its natural host. In particular the immunological events occurring in the primary infection and in the establishment of latency are poorly understood. The virus infects experimental mice, replicating in the lung. Spread then occurs to the B-cell compartment resulting in splenomegaly, a process reminiscent of infectious mononucleosis in humans. The virus then becomes latent in B cells and persists. In addition, long-term infection is associated with the development of lymphoproliferative disease. We show here that CD8 T cells are key cells in resolving the primary infection and in maintaining the numbers of latently-infected B cells. A critical interplay exists between B cells and CD4 T cells in the genesis of splenomegaly and in the numbers of latently infected B cells. Cytokines are probably involved here and serve to induce cell expansion in the spleen. A number of genes have been identified and probes for the lytic and latent cycle are being developed. The use of recombinant proteins, recombinant viruses and knockout mice will facilitate the use of this model in the exploration of immunotherapeutic strategies to target lytic and latent infections by gammaherpesvirus.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 2","pages":"Pages 125-130"},"PeriodicalIF":0.0,"publicationDate":"1996-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51136555","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}

引用次数: 26

Lymphocyte-dependent ‘natural’ immunity to virus infections mediated by both natural killer cells and memory T cells 淋巴细胞对由自然杀伤细胞和记忆T细胞介导的病毒感染的依赖性“自然”免疫

Seminars in virology Pub Date : 1996-04-01 DOI: 10.1006/smvy.1996.0012

Raymond M. Welsh, Chin H. Tay, Steven M. Varga, Carey L. O'Donnell, Kristin L. Vergilis, Liisa K. Selin

{"title":"Lymphocyte-dependent ‘natural’ immunity to virus infections mediated by both natural killer cells and memory T cells","authors":"Raymond M. Welsh, Chin H. Tay, Steven M. Varga, Carey L. O'Donnell, Kristin L. Vergilis, Liisa K. Selin","doi":"10.1006/smvy.1996.0012","DOIUrl":"10.1006/smvy.1996.0012","url":null,"abstract":"<div><p>The replication and dissemination of viruses in the host can be retarded at early stages of infection by lymphocytes not previously exposed to the invading pathogen. Natural killer (NK) cells responding to virus-induced cytokines can mediate profound antiviral effects. Studies with murine cytomegalovirus suggest that NK cells may mediate anti-viral functions by different mechanisms in different organs. T cells may also mediate a rapidly-inducible natural immunity against viral infections. A subpopulation of memory T cells specific for one infectious agent may be stimulated through crossreactive determinants encoded by a heterologous infectious agent and thereby play an active role in the early host response to infection. This heterologous T cell-dependent ‘natural’ immunity may in part be due to the liberation of antiviral cytokines such as interferon γ, as there is much higher production of this cytokine early in infection in mice immune and previously exposed to heterologous infectious agents. Thus, both NK cells and memory T cells may act early in infection to delay the spread of virus, allowing time for high affinity antigen-specific responses to develop and cure the host of infection.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 2","pages":"Pages 95-102"},"PeriodicalIF":0.0,"publicationDate":"1996-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51135879","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}

引用次数: 17

Endogenous ecotropic and recombinant MCF mouse retroviral variation and escape from antiviral CTL 内源性亲生态和重组MCF小鼠逆转录病毒变异和抗病毒CTL的逃逸

Seminars in virology Pub Date : 1996-02-01 DOI: 10.1006/smvy.1996.0007

William R. Green, Patrick M. Smith

引用次数: 10

Cytotoxic T-cell antagonism in HIV-1 HIV-1细胞毒性t细胞的拮抗作用

Seminars in virology Pub Date : 1996-02-01 DOI: 10.1006/smvy.1996.0005

Paul Klenerman, Rodney Phillips, Andrew McMichael

引用次数: 16

Immunobiology of cytotoxic T-cell resistant virus variants: studies on lymphocytic choriomeningitis virus (LCMV) 细胞毒性t细胞耐药病毒变异的免疫生物学:淋巴细胞性脉络丛脑膜炎病毒(LCMV)的研究

Seminars in virology Pub Date : 1996-02-01 DOI: 10.1006/smvy.1996.0002

Demetrius Moskophidis , Rolf M. Zinkernagel*

{"title":"Immunobiology of cytotoxic T-cell resistant virus variants: studies on lymphocytic choriomeningitis virus (LCMV)","authors":"Demetrius Moskophidis , Rolf M. Zinkernagel*","doi":"10.1006/smvy.1996.0002","DOIUrl":"10.1006/smvy.1996.0002","url":null,"abstract":"<div><p>Replication of the genetically variable lymphocytic choriomeningitis virus (LCMV) gives rise to a pool of variant viruses. Under the selection pressure exerted by a strong but narrow repertoire of antiviral cytotoxic T-cells (CTL) i.e. monoclonal or polyclonal monoepitope, variant viruses emerge that contain point mutations in the nucleotide sequence encoding antigenic CTL epitopes; these variants can be selected in both infected mice and cell cultures. These mutations permit infected cells to escape CTL recognition by altering the ability of the mutant peptides to bind MHC class-I-molecules or by interfering with the ability of T-cell receptors to interact with the mutant peptide/MHC complex. Because viral infections often trigger a polyclonal repertoire of antiviral CTL to multiple epitopes, the likelihood of selection of CTL resistant variants is probably low, but not impossible. Our empirical observations suggest that antigenic variations, even if they only occur in a part of the available CTL epitope, may exert significant effects on the subtle biological equilibrium established between virus and host immune system. This can reduce immunological control of the pathogen population, and so permit persistence of viral infection and promote disease progression.</p></div>","PeriodicalId":92955,"journal":{"name":"Seminars in virology","volume":"7 1","pages":"Pages 3-11"},"PeriodicalIF":0.0,"publicationDate":"1996-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/smvy.1996.0002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51135466","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}

引用次数: 9