Abstract

Many high-consequence human and animal pathogens persist in wildlife reservoirs. An understanding of the dynamics of these pathogens in their reservoir hosts is crucial to inform the risk of spill-over events, yet our understanding of these dynamics is frequently insufficient. Viral persistence in a wild bat population was investigated by combining empirical data and in-silico analyses to test hypotheses on mechanisms for viral persistence. A fatal zoonotic virus, European Bat lyssavirus type 2 (EBLV-2), in Daubenton’s bats (Myotis daubentonii) was used as a model system. A total of 1839 M. daubentonii were sampled for evidence of virus exposure and excretion during a prospective nine year serial cross-sectional survey. Multivariable statistical models demonstrated age-related differences in seroprevalence, with significant variation in seropositivity over time and among roosts. An Approximate Bayesian Computation approach was used to model the infection dynamics incorporating the known host ecology. The results demonstrate that EBLV-2 is endemic in the study population, and suggest that mixing between roosts during seasonal swarming events is necessary to maintain EBLV-2 in the population. These findings contribute to understanding how bat viruses can persist despite low prevalence of infection, and why infection is constrained to certain bat species in multispecies roosts and ecosystems.

Highlights

  • Rabies virus is one of a growing number of recognised lyssavirus species that are all capable of causing fatal encephalitis[4]

  • The low frequency of detected virus excretion and relatively short infectious periods suggest that the mechanism of maintenance of infection within a reservoir population is not resolved and has led to suggestions that the viral infection dynamics in bats may differ fundamentally from those in terrestrial carnivores

  • Following removal of samples with insufficient volume or quality, 1839 serum samples were suitable for testing for anti-European bat lyssavirus type 2 (EBLV-2) antibodies, and 1680 oropharyngeal swabs for virus shedding using PCR and virus culture

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Summary

Introduction

Rabies virus is one of a growing number of recognised lyssavirus species that are all capable of causing fatal encephalitis[4]. In the absence of detailed disease prevalence data, seroprevalence determined by sampling live bats has been used as a surrogate for EBLV-2 persistence in bat populations[33] This assumes that it is possible for a bat to be exposed to the virus and seroconvert to a level detectable by virus neutralising antibody tests, and that the tests are specific for the virus being studied[34]. Numerous serology studies have shown lyssavirus antibodies in healthy bats leading to the conclusion that they have either successfully controlled infection or been exposed to sufficient virus to seroconvert without active infection in the bat’s nervous system Proposed mechanisms in the latter case include aerosol exposure to virus in the roost[37,38] or repeated exposure to virus during normal roost behaviour such as allogrooming. In the absence of conclusive observational or experimental data regarding mechanisms of persistence in a population, it is necessary to develop and test hypotheses for EBLV-2 transmission and seroconversion through infection dynamics modelling[3]

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