Age-dependency of avian responses to West Nile virus


Meeting Abstract

109.4  Wednesday, Jan. 7 11:00  Age-dependency of avian responses to West Nile virus GERVASI, S.S.*; BINGHAM, A.; BURGAN, S.; UNNASCH, T.; MARTIN, L.B.; University of South Florida steph.gervasi@gmail.com

Ontogenetic variation in traits related to survival can result in age-structured heterogeneity in natural populations. For example, the ability to cope with infectious disease is driven by immunological responses of hosts, which can vary with age and in the context of competing energetic demands. Very young and very old individuals often suffer disproportionately from disease because they are immunologically naive or undergoing immunosenescence. Yet, age-specific responses can be difficult to predict, since differential allocation of resources towards growth, reproduction, and anti-pathogen responses changes throughout an organism’s life. Growing evidence indicates that different age-classes of hosts can contribute uniquely to epidemiological dynamics. Heterogeneity in traits such as susceptibility, vulnerability, and infectiousness can affect whether a pathogen spreads and persists in a host population. Whether age-specific host contributions to disease dynamics arise from variation in exposure or variation in responses to exposure has been difficult to disentangle in observational studies in natural systems. Here, we controlled for variation in exposure by challenging different age cohorts of avian hosts under identical conditions to a standardized dose of an emerging zoonotic pathogen, West Nile virus. We hypothesized that fledged (1-2 month old), recently matured (8-10 month old), and old-aged (> 2-3 year old) Zebra finches (Taeniopygia guttata) would differ in their responses to the virus. More specifically, we predicted that rates of infection, magnitude and duration of viremia, viral shedding, neutralizing antibody responses, and post-infection behavior would depend on age-class affiliation and be mediated via changes in immunity. Age-structure of enzootic hosts in natural populations varies in space and time and may be a key driver of pathogen transmission dynamics and disease risk to humans and wildlife.

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