The cellular adaptive immune response plays a key role in resolving influenza infection. It can provide cross-protection between subtypes of influenza A which share epitopes; thus, the strength of the immune response to a given strain is dependent upon the individual's infectionhistory. We model cross-reactive cellular adaptive immune responses induced by multiple infections, and show how the formation and re-activation of memory T cells explains observed shortening of a second infection when cross-reactivity is present . We include three possible mechanisms which determine the strength of the cross-reactive immune response . Our model of cross-reactivity contributes to understanding how repeated exposures change an individual's immune profile over a lifetime .
The cellular adaptive immune response plays a key role in resolving influenza infection. Experiments where individuals are successively infected with different strains within a short timeframe provide insight into the underlying viral dynamics and the role of a cross-reactive immune response in resolving an acute infection. We construct a mathematical model of within-host influenza viral dynamics including three possible factors which determine the strength of the cross-reactive cellular adaptive immune response: the initial naive T cell number, the avidity of the interaction between T cells and the epitopes presented by infected cells, and the epitope abundance per infected cell. Our model explains the experimentally observed shortening of a second infection when cross-reactivity is present , and shows that memory in the cellular adaptive immune response is necessary to protect against a second infection .
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It can provide cross-protection between subtypes of influenza A which share epitopes; thus, the strength of the immune response to a given strain is dependent upon the individual's infectionhistory. We model
Experiments where individuals are successively infected with different strains within a short timeframe provide insight into the underlying viral dynamics and the role of a cross-reactive immune response in resolving an acute infection. We construct a mathematical model of within-host influenza viral dynamics including three possible factors which determine the strength of the
R
responses induced by multiple infections, and show how the formation and re-activation of memory T cells explains
response: the initial naive T cell number, the avidity of the interaction between T cells and the epitopes presented by infected cells, and the epitope abundance per infected cell. Our model explains the experimentally
R
. We include three possible mechanisms which determine the strength of the cross-reactive immune response . Our model of cross-reactivity contributes to understanding how repeated exposures change an individual's immune profile over a lifetime
, and shows that memory in the cellular adaptive immune response is necessary to protect against a second infection