Mechanisms of Disease Production: Acute Infections
Identifieur interne : 000973 ( Pmc/Checkpoint ); précédent : 000972; suivant : 000974Mechanisms of Disease Production: Acute Infections
Auteurs : Frank FennerSource :
- Veterinary Virology ; 1987.
Abstract
This chapter discusses the ways in which viral replication damages tissues and organs and the ways in which the body's own responses may cause damage. It presents examples illustrating the pathogenesis of four basic kinds of acute viral infection: respiratory, intestinal, generalized, and neurological. As the immune system plays a key role in protection against infections, viral damage to its components can exacerbate the severity of disease or predispose to superinfection with other viral or nonviral agents. Both specific acquired immunodeficiency and generalized immunosuppression can occur in viral infections. The immune response to viral infection may itself frequently contribute to the pathology of the disease. Inflammation with accompanying cellular infiltration is a regular feature of viral infection. Such common signs as erythema, edema, and enlargement of lymph nodes have an immunological basis. There are viral diseases in which the cardinal manifestations are caused by the body's immune response. Immunopathological (hypersensitivity) reactions are traditionally classified into types 1, 2, 3, and 4. For most viral infections, it is not known whether immunopathological effects make a significant contribution to disease and if so then as to which of the four classical hypersensitivity reactions is implicated. It is instructive to speculate about the possible involvement of different kinds of hypersensitivity reactions in viral diseases.
Url:
DOI: 10.1016/B978-0-12-253055-5.50014-1
PubMed: NONE
PubMed Central: 7149365
Affiliations:
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Veterinary Virology</journal-id><journal-title-group><journal-title>Veterinary Virology</journal-title></journal-title-group></journal-meta><article-meta><article-id pub-id-type="pmc">7149365</article-id><article-id pub-id-type="publisher-id">B978-0-12-253055-5.50014-1</article-id><article-id pub-id-type="doi">10.1016/B978-0-12-253055-5.50014-1</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Mechanisms of Disease Production: Acute Infections</article-title></title-group><contrib-group><contrib contrib-type="author" id="au1"><name><surname>FENNER</surname><given-names>FRANK</given-names></name></contrib></contrib-group><aff id="aff1">The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia</aff><contrib-group><contrib contrib-type="author" id="au2"><name><surname>BACHMANN</surname><given-names>PETER A.</given-names></name></contrib></contrib-group><aff id="aff2">Institut für Medizinische Mikrobiologie, Infektions -und Seuchenmedizin, Ludwig-Maximilians-Universität, Munich, Federal Republic of Germany</aff><contrib-group><contrib contrib-type="author" id="au3"><name><surname>GIBBS</surname><given-names>E. PAUL J.</given-names></name></contrib></contrib-group><aff id="aff3">College of Veterinary Medicine, University of Florida, Gainesville, Florida</aff><contrib-group><contrib contrib-type="author" id="au4"><name><surname>MURPHY</surname><given-names>FREDERICK A.</given-names></name></contrib></contrib-group><aff id="aff4">Division of Viral Diseases, Centers for Disease Control, Atlanta, Georgia</aff><contrib-group><contrib contrib-type="author" id="au5"><name><surname>STUDDERT</surname><given-names>MICHAEL J.</given-names></name></contrib></contrib-group><aff id="aff5">Virus Laboratory, School of Veterinary Science, University of Melbourne, Melbourne, Victoria, Australia</aff><contrib-group><contrib contrib-type="author" id="au6"><name><surname>WHITE</surname><given-names>DAVID O.</given-names></name></contrib></contrib-group><aff id="aff6">Department of Microbiology, University of Melbourne, Melbourne, Victoria, Australia</aff><pub-date pub-type="pmc-release"><day>27</day><month>6</month><year>2014</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><year>1987</year></pub-date><pub-date pub-type="epub"><day>27</day><month>6</month><year>2014</year></pub-date><fpage>183</fpage><lpage>202</lpage><permissions><copyright-statement>Copyright © 1987 ACADEMIC PRESS, INC. Published by Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>1987</copyright-year><copyright-holder>ACADEMIC PRESS, INC.</copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="ceabs10a"><title>Publisher Summary</title><p>This chapter discusses the ways in which viral replication damages tissues and organs and the ways in which the body's own responses may cause damage. It presents examples illustrating the pathogenesis of four basic kinds of acute viral infection: respiratory, intestinal, generalized, and neurological. As the immune system plays a key role in protection against infections, viral damage to its components can exacerbate the severity of disease or predispose to superinfection with other viral or nonviral agents. Both specific acquired immunodeficiency and generalized immunosuppression can occur in viral infections. The immune response to viral infection may itself frequently contribute to the pathology of the disease. Inflammation with accompanying cellular infiltration is a regular feature of viral infection. Such common signs as erythema, edema, and enlargement of lymph nodes have an immunological basis. There are viral diseases in which the cardinal manifestations are caused by the body's immune response. Immunopathological (hypersensitivity) reactions are traditionally classified into types 1, 2, 3, and 4. For most viral infections, it is not known whether immunopathological effects make a significant contribution to disease and if so then as to which of the four classical hypersensitivity reactions is implicated. It is instructive to speculate about the possible involvement of different kinds of hypersensitivity reactions in viral diseases.</p></abstract></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Fenner, Frank" sort="Fenner, Frank" uniqKey="Fenner F" first="Frank" last="Fenner">Frank Fenner</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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