Kinetics of influenza A virus infections in a heterogeneous cell population

Several mechanisms have been proposed to account for the marked increase in severity of human infections with avian influenza compared to human influenza strains, including increased cytokine expression, poor immune response, and differences in target cell receptor affinity. Here, the effect of target cell tropism on disease severity is studied using a mathematical model for in-host influenza viral infection in a cell population consisting of two different cell types.  The two cell types differ only in their susceptibility to infection and rate of viral production. We show the existence of a parameter regime which is characterized by high viral loads sustained long after the onset of infection. This finding suggests that cell tropism alone is sufficient to explain the increase in infection severity of certain strains of the influenza A virus. The implications of this finding for antiviral treatment strategies will be discussed.