Speaker
Description
Reinfections with respiratory viruses are thought to be driven by ongoing antigenic immune escape in the viral population. However, this does not explain why antigenic variation is frequently observed in respiratory viruses and not systemically replicating viruses. Here, we argue that the rapid rate of waning immunity in the respiratory tract is a key driver of antigenic evolution in respiratory viruses. Waning immunity results in hosts with immunity levels that protect against homologous reinfection but are insufficient to protect against infection with an antigenically different (heterologous) strain. Thus, when partially immune hosts are present at a high enough density, an immune escape variant can invade the viral population even though that variant cannot infect solidly immune hosts.
We then examine the consequences of waning immunity driven by antigenic changes for the extent of pathology at the population level. Our models incorporate how susceptibility, infectivity and pathology depend on the level of immunity of the individual. We use the model to explore how the total disease burden (number of severe cases) depends on the extent of transmission of the pathogen and the rate of waning of immunity. We explore scenarios where reducing transmission can increase disease burden. We then consider the implications for vaccination and specifically when targeted vaccination could be more effective than mass vaccination.
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