Abstract
Abstract Seasonal influenza and the risk of widespread influenza pandemics are an ongoing major world health concern. In the United States alone, influenza infection results in more than 200,000 hospitalizations and up to 41,000 deaths each year. The current vaccine strategies focus on eliciting neutralizing antibodies against hemagglutinin and neuraminidase, the major surface glycoproteins involved with viral entry and exit from a host cell. Because of the highly mutable nature of influenza, the vaccine must be reformulated each year - highlighting the necessity for an alternate approach that provides broad and long-lasting protection. We have approached this problem by asking if CD4 T cell memory, elicited by peptide priming, is sufficient to accelerate T cell and B cell responses to influenza infection. After immunization with immunogenic peptides derived from A/New Caledonia/20/99 followed by infection with the same virus, we observed an increased frequency of virus specific CD4 T cells 7 days post infection. Additionally, there was an enhanced B cell response both kinetically and in magnitude. We have also observed a strong correlation between the frequencies of follicular T helper cells and germinal center B cells in the peptide primed/infected cohorts that are not seen in the control primed/infected group. Our results suggest that T cell help for a primary B cell response to infection is limiting, and that peptide priming is sufficient to generate a functional memory CD4 pool.
Published Version
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