Front Immunol. 7:611 (2016) Myriad experiments have identified an important role for $\rm CD8^+$ T cell
response mechanisms in determining recovery from influenza A virus infection.
Animal models of ...influenza infection further implicate multiple elements of the
immune response in defining the dynamical characteristics of viral infection.
To date, influenza virus models, while capturing particular aspects of the
natural infection history, have been unable to reproduce the full gamut of
observed viral kinetic behaviour in a single coherent framework. Here, we
introduce a mathematical model of influenza viral dynamics incorporating all
major immune components (innate, humoral and cellular) and explore its
properties with a particular emphasis on the role of cellular immunity.
Calibrated against a range of murine data, our model is capable of
recapitulating observed viral kinetics from a multitude of experiments.
Importantly, the model predicts a robust exponential relationship between the
level of effector $\rm CD8^+$ T cells and recovery time, whereby recovery time
rapidly decreases to a fixed minimum recovery time with an increasing level of
effector $\rm CD8^+$ T cells. We find support for this relationship in recent
clinical data from influenza A(H7N9) hospitalised patients. The exponential
relationship implies that people with a lower level of naive $\rm CD8^+$ T
cells may receive significantly more benefit from induction of additional
effector $\rm CD8^+$ T cells arising from immunological memory, itself
established through either previous viral infection or T cell-based vaccines.
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.
...both children who had lateral neck x ray films done had these from the emergency department of their local (different) district general hospitals before being referred to our tertiary service. ...Approximately one third have minor immunoglobulin abnormalities of uncertain clinical relevance. 2 Most mount a convalescent antibody response to disease of a magnitude consistent with priming in infancy, indicating that vaccine induced immunity has failed to protect. 3 Hib antibody concentrations wane rapidly after the primary course of immunisation, 4 and in the absence of a fourth dose of vaccine British children are heavily dependent on B cell memory to prevent disease.
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