PMC:7551987 / 28535-32089 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7551987","sourcedb":"PMC","sourceid":"7551987","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7551987","text":"Practical Implications for the Understanding of Outbreaks Caused by Emerging Viruses\nThat different features of an outbreak are differentially influenced by the endpoints of viral life-history evolution highlights how epidemiology should continue to consider principles in the evolution and ecology of infectious disease in its analyses and predictions. As not all features of an epidemic are going to be equally reliable signatures of virus evolution, we should carefully consider the data on how the dynamics of an epidemic change when making inferences about whether a pathogen population is essentially different from prior iterations (e.g., prior outbreaks of the same virus type). The results of this study suggest that carefully constructed, mechanistically sound models of epidemics are important, both for capturing the dynamics of an outbreak and for abetting our efforts to understand how evolution of survival and virulence influences disease dynamics.\nFor example, the potential for adaptive evolution of SARS-CoV-2 has emerged as a possible explanation for different COVID-19 dynamics in different countries. We suggest that such interpretations should be considered with caution and that they require very specific types of evidence to support them. As of 1 July 2020, any conclusion that widespread SARS-CoV-2 evolution is an explanation for variation in disease patterns across settings (space and/or time) is premature.\nThe practical process of interpreting the evolutionary consequences of signals of virus evolution should encompass several discrete steps. Firstly, we should determine whether molecular signatures exist for adaptive evolution. Adaptive evolution would manifest in observable differences in genotype and phenotype and, perhaps, in the natural history of disease. Secondly, we should aim to attain knowledge of the underlying mechanistic relationship between survival and virulence. This knowledge is not necessarily easy to attain (it requires extensive laboratory studies) but would allow added biological insight: we may be able to extrapolate how changes in some traits (e.g., those that compose survival) influence others (e.g., those that influence virulence).\nMore generally, our findings suggest that the ability to detect the consequences of virus evolution would depend on which feature of an outbreak an epidemiologist measures: from our analysis, R0 is most impacted by changes in virulence and survival. In addition, the total number of infected individuals in the early window and the size of the infected “peak” would each be impacted most readily by changes in virulence–survival traits. The rate at which the epidemic peak was reached, on the other hand, showed relatively little change as survival increased or between the two correlation scenarios. Consequently, it would not serve as a useful proxy for virus evolution.\nWhile the stochastic, sometimes entropic nature of epidemics renders them very challenging to predict [36], we suggest that canons such as life-history theory and the evolution of virulence provide useful lenses that can aid in our ability to interpret how life-history changes in virus populations will manifest at the epidemiological scale. We propose that, in an age of accumulating genomic and phenotypic data in many pathogen–host systems, we continue to responsibly apply or modify existing theory in order to collate said data into an organized picture for how different components of the host–parasite interaction influence the shape of viral outbreaks of various 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