| In vivo impact of cytomegalovirus evasion of CD8 T-cell immunity: Facts and thoughts based on murine models. | |
| | |
MedLine Citation:
|
PMID: 20933556 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
|
Cytomegaloviruses (CMVs) co-exist with their respective host species and have evolved to avoid their elimination by the hosts' immune effector mechanisms and to persist in a non-replicative state, known as viral latency. There is evidence to suggest that latency is nevertheless a highly dynamic condition during which episodes of viral gene desilencing, which can be viewed as incomplete reactivations, cause intermittent antigenic activity that stimulates CD8 memory-effector T cells and drives their clonal expansion. These T cells are supposed to terminate reactivation before completion of the productive viral cycle. In this view, CMVs do not "evade" their respective host's immune response but are actually held in check all the time, unless the host gets immunocompromised. Accordingly, CMV disease is typically a disease of the immunocompromised host only. Here we review current knowledge about the in vivo role of viral proteins involved in subverting the immune recognition of infected cells with focus on the CD8 T-cell response and viral interference with the MHC class-I pathway of antigenic peptide presentation. Whereas the intracellular functions of these "immune-evasion proteins" are known in molecular detail, knowledge of their in vivo role in CMV biology is only beginning to take shape. Experimental studies on the in vivo function of human CMV (hCMV) immune-evasion proteins prohibits, of course. Studying animal CMVs paradigmatically in the corresponding natural host is therefore used to identify principles from which the role of hCMV immune-evasion proteins can hopefully be inferred. Here we summarize recent insights gained primarily from the murine model. |
| | |
Authors:
|
Niels A W Lemmermann; Verena Böhm; Rafaela Holtappels; Matthias J Reddehase |
Related Documents
:
|
16750166 - Down-regulation of the nkg2d ligand mica by the human cytomegalovirus glycoprotein ul142. 20646766 - The immune response of foals to natural infection with equid herpesvirus-2 and its asso... 10816366 - Competitive coexistence in antiviral immunity. 11502076 - Breach of il-12 monopoly in the initiation of type 1 immunity to intracellular infectio... 15683586 - Inflammation, blood pressure, and stroke: an opportunity to target primary prevention? 22547346 - Induced expression of stim1 sensitizes intestinal epithelial cells to apoptosis by modu... |
Publication Detail:
|
Type: Journal Article Date: 2010-10-08 |
Journal Detail:
|
Title: Virus research Volume: 157 ISSN: 1872-7492 ISO Abbreviation: Virus Res. Publication Date: 2011 May |
Date Detail:
|
Created Date: 2011-04-25 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 8410979 Medline TA: Virus Res Country: Netherlands |
Other Details:
|
Languages: eng Pagination: 161-74 Citation Subset: IM |
Copyright Information:
|
Copyright © 2010 Elsevier B.V. All rights reserved. |
Affiliation:
|
Institute for Virology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Identification of an amino acid domain encoded by the capsid gene of porcine circovirus type 2 that ...
Next Document: Molecular imaging with SPECT as a tool for drug development.