tetano
Editor, Senior Moderator
J Virol. 2011 Oct 5. [Epub ahead of print]
Infection with seasonal influenza virus elicits CD4 T cells specific for genetically conserved epitopes that can be rapidly mobilized for protective immunity to pandemic H1N1 influenza.
Alam S, Sant AJ.
Source
David H. Smith Center for Vaccine Biology and Immunology, University of Rochester Medical Center, Rochester, New York 14642.
Abstract
In recent years, influenza viruses with pandemic potential have been a major concern worldwide. One unresolved issue is how infection or vaccination with seasonal influenza strains influences the ability to elicit a protective immune response to novel pandemic strains. In this study, we developed a mouse model of primary and secondary influenza infection, using a widely circulating seasonal H1N1 virus and the pandemic strain of H1N1 that emerged in Mexico in 2009, and evaluated several key issues. First, using overlapping peptide libraries encompassing the entire translated sequences of 5 major influenza proteins, we assessed the specificity of CD4 T cell reactivity toward epitopes conserved among H1N1 viruses or unique to the seasonal and pandemic strain using EliSpot assays. Our data show CD4 T cells that are reactive to both virus-specific and genetically conserved epitopes are elicited, allowing separate tracking of these responses. Cross-reactive CD4 T cells generated from seasonal influenza infection were found to expand earlier after secondary infection with pandemic H1N1 than CD4 T cells specific for new epitopes. Coincident with this rapid CD4 T cell response was a potentiated neutralizing antibody response to the pandemic strain and protection from the pathological effects of infection with the pandemic virus. This protection was not dependent on CD8 T cells. Together our results indicate that exposure to seasonal vaccines and infection elicits CD4 T cells that promote the ability of the mammalian host to mount a protective immune response to pandemic strains of influenza.
PMID:
21976658
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21976658
Infection with seasonal influenza virus elicits CD4 T cells specific for genetically conserved epitopes that can be rapidly mobilized for protective immunity to pandemic H1N1 influenza.
Alam S, Sant AJ.
Source
David H. Smith Center for Vaccine Biology and Immunology, University of Rochester Medical Center, Rochester, New York 14642.
Abstract
In recent years, influenza viruses with pandemic potential have been a major concern worldwide. One unresolved issue is how infection or vaccination with seasonal influenza strains influences the ability to elicit a protective immune response to novel pandemic strains. In this study, we developed a mouse model of primary and secondary influenza infection, using a widely circulating seasonal H1N1 virus and the pandemic strain of H1N1 that emerged in Mexico in 2009, and evaluated several key issues. First, using overlapping peptide libraries encompassing the entire translated sequences of 5 major influenza proteins, we assessed the specificity of CD4 T cell reactivity toward epitopes conserved among H1N1 viruses or unique to the seasonal and pandemic strain using EliSpot assays. Our data show CD4 T cells that are reactive to both virus-specific and genetically conserved epitopes are elicited, allowing separate tracking of these responses. Cross-reactive CD4 T cells generated from seasonal influenza infection were found to expand earlier after secondary infection with pandemic H1N1 than CD4 T cells specific for new epitopes. Coincident with this rapid CD4 T cell response was a potentiated neutralizing antibody response to the pandemic strain and protection from the pathological effects of infection with the pandemic virus. This protection was not dependent on CD8 T cells. Together our results indicate that exposure to seasonal vaccines and infection elicits CD4 T cells that promote the ability of the mammalian host to mount a protective immune response to pandemic strains of influenza.
PMID:
21976658
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21976658