Acute emergence and reversion of influenza A virus quasispecies within CD8+ T cell antigenic peptides

Sophie A. Valkenburg, Sergio Quiñones-Parra, Stephanie Gras, Naomi Komadina, Jodie McVernon, Zhongfang Wang, Hanim Halim, Pina Iannello, Catherine Cole, Karen Laurie, Anne Kelso, Jamie Rossjohn, Peter C. Doherty, Stephen J. Turner and Katherine Kedzierska ()
Additional contact information
Sophie A. Valkenburg: University of Melbourne
Sergio Quiñones-Parra: University of Melbourne
Stephanie Gras: School of Biomedical Sciences, Monash University
Naomi Komadina: WHO Collaborating Centre for Reference and Research on Influenza
Jodie McVernon: Melbourne School of Population and Global Health, the University of Melbourne
Zhongfang Wang: University of Melbourne
Hanim Halim: School of Biomedical Sciences, Monash University
Pina Iannello: WHO Collaborating Centre for Reference and Research on Influenza
Catherine Cole: School of Paediatrics and Child Health, University of Western
Karen Laurie: WHO Collaborating Centre for Reference and Research on Influenza
Anne Kelso: WHO Collaborating Centre for Reference and Research on Influenza
Jamie Rossjohn: School of Biomedical Sciences, Monash University
Peter C. Doherty: University of Melbourne
Stephen J. Turner: University of Melbourne
Katherine Kedzierska: University of Melbourne

Nature Communications, 2013, vol. 4, issue 1, 1-10

Abstract: Abstract Influenza A virus-specific CD8+ cytotoxic T lymphocytes (CTLs) provide a degree of cross-strain protection that is potentially subverted by mutation. Here we describe the sequential emergence of such variants within CTL epitopes for a persistently infected, immunocompromised infant. Further analysis in immunodeficient and wild-type mice supports the view that CTL escape variants arise frequently in influenza, accumulate with time and revert in the absence of immune pressure under MHCI-mismatched conditions. Viral fitness, the abundance of endogenous CD8+ T cell responses and T cell receptor repertoire diversity influence the nature of these de novo mutants. Structural characterization of dominant escape variants shows how the peptide–MHCI interaction is modified to affect variant-MHCI stability. The mechanism of influenza virus escape thus looks comparable to that recognized for chronic RNA viruses like HIV and HCV, suggesting that immunocompromised patients with prolonged viral infection could have an important part in the emergence of influenza quasispecies.

Date: 2013
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms3663 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3663

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms3663

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().