Abstract
Pathogens causing acute disease and death or lasting immunity require specific spatial or temporal processes to persist in populations. Host traits, such as maternally-derived antibody (MDA) and seasonal birthing affect infection maintenance within populations. Our study objective is to understand how viral and host traits lead to population level infection persistence when the infection can be fatal. We collected data on African fruit bats and a rabies-related virus, Lagos bat virus (LBV), including through captive studies. We incorporate these data into a mechanistic model of LBV transmission to determine how host traits, including MDA and seasonal birthing, and viral traits, such as incubation periods, interact to allow fatal viruses to persist within bat populations. Captive bat studies supported MDA presence estimated from field data. Captive bat infection-derived antibody decayed more slowly than MDA, and while faster than estimates from the field, supports field data that suggest antibody persistence may be lifelong. Unobserved parameters were estimated by particle filtering and suggest only a small proportion of bats die of disease. Pathogen persistence in the population is sensitive to this proportion, along with MDA duration and incubation period. Our analyses suggest MDA produced bats and prolonged virus incubation periods allow viral maintenance in adverse conditions, such as a lethal pathogen or strongly seasonal resource availability for the pathogen in the form of seasonally pulsed birthing.
Highlights
Understanding what mechanisms allow maintenance of infections within populations is fundamental to disease ecology [1, 2]
We previously described the use of a periodic Gaussian function (PGF) that allows births to be pulsed over a period and ensures that no births occur outside the birthing season, B(t) = κexp[−scos2] [2, 39]
Lyssavirus RNA was not detected by RT-qPCR from the throat swabs of any bat on entry to the captive colony, nor was lyssavirus detected in the brains of nine captive bats that died during the study period
Summary
Understanding what mechanisms allow maintenance of infections within populations is fundamental to disease ecology [1, 2]. In a study of RABV in tropical vampire bats (Desmodus rotundus), models fit to spatially replicated, longitudinal field seroprevalence data supported findings that most RABV exposures are non-fatal and concluded dispersal was necessary to allow RABV persistence at the population level [25]. These studies suggest spatially or temporally variable resources that determine host population dynamics may be driving RABV dynamics. We hypothesise that duration of immunity, combined with slow infection dynamics, may be key factors in the maintenance of LBV within closed populations of bats To test this hypothesis, we incorporate epidemiological, immunological and ecological data on LBV in E. helvum into a stochastic disease dynamic model. We use a range of sensitivity analyses to help elucidate the host and pathogen traits that allow LBV infection to persist in E. helvum populations
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