RESUMO
West Nile Virus (WNV) is a mosquito-borne pathogen that primarily infects birds. Infections can spillover to humans and cause a spectrum of clinical symptoms, including WNV neuroinvasive disease. The extrinsic incubation period (EIP) is the time taken for a mosquito to become infectious following the ingestion of an infected blood meal. Characterising how the EIP varies with temperature is an essential part of predicting the impact and transmission dynamics of WNV. We re-analyse existing experimental data using Bayesian time delay models, allowing us to account for variation in how quickly individual mosquitoes become infectious with WNV. In these experiments, cohorts of Culex pipiens mosquitoes were infected with WNV and kept under different temperature conditions, being checked for disseminated infection at defined timepoints. We find that EIPs are best described with a Weibull distribution and become shorter log-linearly with temperature. Under 18ºC, less than 1% of infected Cx. pipiens had a disseminated infection after 5 days, compared to 9.73% (95% CrI: 7.97 to 11.54) at 25ºC and 42.20% (95% CrI: 38.32 to 46.60) at 30ºC. In the hottest experimental temperature treatment (32ºC), the EIP50 was estimated at 3.78 days (CrI: 3.42 to 4.15) compared to over 100 days in the coolest treatment (15ºC). The variance of EIPs was found to be much larger at lower temperatures than higher temperatures, highlighting the importance of characterising the time delay distribution associated with the EIP. We additionally demonstrate a competitive advantage of WNV strain WN02 over NY99, where the former infects mosquitoes more quickly at colder temperature than the latter. This research contributes crucial parameters to the WNV literature, providing essential insights for modellers and those planning interventions.
RESUMO
Until the early twentieth century, populations on many Pacific Islands had never experienced measles. As travel to the Pacific Islands by Europeans became more common, the arrival of measles and other pathogens had devastating consequences. In 1911, Rotuma in Fiji was hit by a measles epidemic, which killed 13% of the island population. Detailed records show two mortality peaks, with individuals reported as dying solely from measles in the first and from measles and diarrhoea in the second. Measles is known to disrupt immune system function. Here, we investigate whether the pattern of mortality on Rotuma in 1911 was a consequence of the immunosuppressive effects of measles. We use a compartmental model to simulate measles infection and immunosuppression. Whilst immunosuppressed, we assume that individuals are vulnerable to dysfunctional reactions triggered by either (i) a newly introduced infectious agent arriving at the same time as measles or (ii) microbes already present in the population in a pre-existing equilibrium state. We show that both forms of the immunosuppression model provide a plausible fit to the data and that the inclusion of immunosuppression in the model leads to more realistic estimates of measles epidemiological parameters than when immunosuppression is not included.
