Abstract
1 Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, Mueller Laboratory, University Park, Pennsylvania, United States of America, 2 Fogarty International Center, National Institutes of Health, Bethesda, Maryland, United States of America, 3 Department of Ecology and Evolutionary Biology and Woodrow Wilson School, Princeton University, Princeton, New Jersey, United States of America
Highlights
Pathogen discovery is a major focus of this new-scale genome sequencing [2]
We argue here that the field of viral phylodynamics requires its own discovery phase; that is, a comprehensive and quantitative analysis of the interaction between the ecological and evolutionary dynamics of all circulating RNA viruses from the molecular to the global scale
It is striking that so few complete genome sequences are currently available for viruses whose epidemiological dynamics are known in exquisite detail, such as measles [9,10]; these sequences have been so sparsely sampled in both time and space that a full phylodynamic perspective has not yet been achieved
Summary
The advent of extremely high throughput DNA sequencing ensures that genomic data from microbial organisms can be acquired in unprecedented quantities and with remarkable rapidity. It is only the first step in developing a full quantitative understanding of the processes that shape the epidemiology and evolution— the phylodynamics—of RNA virus infections [8] To achieve this goal, we argue here that the field of viral phylodynamics requires its own discovery phase; that is, a comprehensive and quantitative analysis of the interaction between the ecological and evolutionary dynamics of all circulating RNA viruses from the molecular to the global scale. We argue here that the field of viral phylodynamics requires its own discovery phase; that is, a comprehensive and quantitative analysis of the interaction between the ecological and evolutionary dynamics of all circulating RNA viruses from the molecular to the global scale Such a marriage of phylogenetic and epidemiological dynamics is currently only potentially possible for the select few human viruses for which large genome sequence datasets have been acquired, such as HIV and influenza A virus, and even here fundamental gaps in our knowledge remain (see below). Such a bias against viruses sampled from individuals with asymptomatic infections is a common problem in molecular epidemiology
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