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• W2173519990 endingPage "e0142170" @default.
• W2173519990 startingPage "e0142170" @default.
• W2173519990 abstract "Many human infectious diseases are caused by pathogens that have multiple strains and show oscillation in infection incidence and alternation of dominant strains which together are referred to as epidemic cycling. Understanding the underlying mechanisms of epidemic cycling is essential for forecasting outbreaks of epidemics and therefore important for public health planning. Current theoretical effort is mainly focused on the factors that are extrinsic to the pathogens themselves (extrinsic factors) such as environmental variation and seasonal change in human behaviours and susceptibility. Nevertheless, co-circulation of different strains of a pathogen was usually observed and thus strains interact with one another within concurrent infection and during sequential infection. The existence of these intrinsic factors is common and may be involved in the generation of epidemic cycling of multi-strain pathogens.To explore the mechanisms that are intrinsic to the pathogens themselves (intrinsic factors) for epidemic cycling, we consider a multi-strain SIRS model including cross-immunity and infectivity enhancement and use seasonal influenza as an example to parameterize the model. The Kullback-Leibler information distance was calculated to measure the match between the model outputs and the typical features of seasonal flu (an outbreak duration of 11 weeks and an annual attack rate of 15%). Results show that interactions among strains can generate seasonal influenza with these characteristic features, provided that: the infectivity of a single strain within concurrent infection is enhanced 2-7 times that within a single infection; cross-immunity as a result of past infection is 0.5-0.8 and lasts 2-9 years; while other parameters are within their widely accepted ranges (such as a 2-3 day infectious period and the basic reproductive number of 1.8-3.0). Moreover, the observed alternation of the dominant strain among epidemics emerges naturally from the best fit model. Alternative modelling that also includes seasonal forcing in transmissibility shows that both external mechanisms (i.e. seasonal forcing) and the intrinsic mechanisms (i.e., strain interactions) are equally able to generate the observed time-series in seasonal flu.The intrinsic mechanism of strain interactions alone can generate the observed patterns of seasonal flu epidemics, but according to Kullback-Leibler information distance the importance of extrinsic mechanisms cannot be excluded. The intrinsic mechanism illustrated here to explain seasonal flu may also apply to other infectious diseases caused by polymorphic pathogens." @default.
• W2173519990 created "2016-06-24" @default.
• W2173519990 creator A5005977528 @default.
• W2173519990 date "2015-11-12" @default.
• W2173519990 modified "2023-09-27" @default.
• W2173519990 title "Strain Interactions as a Mechanism for Dominant Strain Alternation and Incidence Oscillation in Infectious Diseases: Seasonal Influenza as a Case Study" @default.
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• W2173519990 doi "https://doi.org/10.1371/journal.pone.0142170" @default.
• W2173519990 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4642928" @default.
• W2173519990 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26562668" @default.
• W2173519990 hasPublicationYear "2015" @default.
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