Protection and compensation in the influenza virus-specific CD8+ T cell response. Webby, Richard J., Andreansky, Samita, Stambas, John, Rehg, Jerold E., Webster, Robert G., Doherty, Peter C. and Turner, Stephen J. 2003, Protection and compensation in the influenza virus-specific CD8+ T cell response., Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 12, pp. 7235-7240, doi: 10.1073/pnas.1232449100. Attached Files Name Description MIMEType Size Downloads Title Protection and compensation in the influenza virus-specific CD8+ T cell response. Author(s) Webby, Richard J. Andreansky, Samita Stambas, John orcid.org/0000-0002-5690-2551 Rehg, Jerold E. Webster, Robert G. Doherty, Peter C. Turner, Stephen J. Journal name Proceedings of the National Academy of Sciences of the United States of America Volume number 100 Issue number 12 Start page 7235 End page 7240 Publisher National Academy of Sciences Place of publication Washington, D.C. Publication date 2003-06 ISSN 0027-8424 1091-6490 Summary Influenza virus-specific CD8+ T cells generally recognize peptides derived from conserved, internal proteins that are not subject to antibody-mediated selection pressure. Prior exposure to any one influenza A virus (H1N1) can prime for a secondary CD8+ T cell response to a serologically different influenza A virus (H3N2). The protection afforded by this recall of established CD8+ T cell memory, although limited, is not negligible. Key characteristics of primary and secondary influenza-specific host responses are probed here with recombinant viruses expressing modified nucleoprotein (NP) and acid polymerase (PA) genes. Point mutations were introduced into the epitopes derived from the NP and PA such that they no longer bound the presenting H2Db MHC class I glycoprotein, and reassortant H1N1 and H3N2 viruses were made by reverse genetics. Conventional (C57BL/6J, H2b, and Ig+/+) and Ig-/- (muMT) mice were more susceptible to challenge with the single NP [HKx31 influenza A virus (HK)-NP] and PA (HK-PA) mutants, but unlike the Ig-/- mice, Ig+/+ mice were surprisingly resistant to the HK-NP/-PA double mutant. This virus was found to promote an enhanced IgG response resulting, perhaps, from the delayed elimination of antigen-presenting cells. Antigen persistence also could explain the increase in size of the minor KbPB1703 CD8+ T cell population in mice infected with the mutant viruses. The extent of such compensation was always partial, giving the impression that any virus-specific CD8+ T cell response operates within constrained limits. It seems that the relationship between protective humoral and cellular immunity is neither simple nor readily predicted. Language eng DOI 10.1073/pnas.1232449100 Field of Research 110804 Medical Virology Socio Economic Objective 920109 Infectious Diseases HERDC Research category C1.1 Refereed article in a scholarly journal Copyright notice ©Copyright 2003, The National Academy of Sciences Persistent URL http://hdl.handle.net/10536/DRO/DU:30028916 Document type: Journal Article Collections: Faculty of Health School of Medicine Related Links Link Description Connect to published version (restricted access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Versions Version Filter Type Wed, 26 May 2010, 16:07:23 EST Fri, 30 Jul 2010, 13:52:45 EST Fri, 30 Jul 2010, 13:53:39 EST Fri, 30 Jul 2010, 13:54:37 EST Fri, 30 Jul 2010, 13:55:37 EST Mon, 16 Jun 2014, 15:50:38 EST Thu, 07 Nov 2019, 14:36:26 EST Fri, 11 Mar 2022, 22:36:45 EST Filtered Full Citation counts:   Cited 102 times in TR Web of Science Cited 108 times in Scopus Search Google Scholar Access Statistics: 855 Abstract Views, 0 File Downloads  -  Detailed Statistics Created: Wed, 26 May 2010, 16:07:23 EST