Viral phylodynamics is defined as the study of how epidemiological, immunological, and evolutionary processes act and potentially interact to shape viral phylogenies.[1]
Since the coining of the term in 2004, research on viral phylodynamics has focused on transmission dynamics in an effort to shed light on how these dynamics impact viral genetic variation. Transmission dynamics can be considered at the level of cells within an infected host, individual hosts within a population, or entire populations of hosts.
Many viruses, especially RNA viruses, rapidly accumulate genetic variation because of short generation times and high mutation rates.
Patterns of viral genetic variation are therefore heavily influenced by how quickly transmission occurs and by which entities transmit to one another.
Patterns of viral genetic variation will also be affected by selection acting on viral phenotypes.
Although viruses can differ with respect to many phenotypes, phylodynamic studies have to date tended to focus on a limited number of viral phenotypes.
These include virulence phenotypes, phenotypes associated with viral transmissibility, cell or tissue tropism phenotypes, and antigenic phenotypes that can facilitate escape from host immunity.
Due to the impact that transmission dynamics and selection can have on viral genetic variation, viral phylogenies can therefore be used to investigate important epidemiological, immunological, and evolutionary processes, such as epidemic spread,[2] spatio-temporal dynamics including metapopulation dynamics,[3] zoonotic transmission, tissue tropism,[4] and antigenic drift.[5]
The quantitative investigation of these processes through the consideration of viral phylogenies is the central aim of viral phylodynamics.
^Bedford T, Cobey S, Beerli P, Pascual M (May 2010). Ferguson NM (ed.). "Global migration dynamics underlie evolution and persistence of human influenza A (H3N2)". PLOS Pathogens. 6 (5): e1000918. doi:10.1371/journal.ppat.1000918. PMC 2877742. PMID 20523898.
^Gray RR, Salemi M, Klenerman P, Pybus OG (2012). Rall GF (ed.). "A new evolutionary model for hepatitis C virus chronic infection". PLOS Pathogens. 8 (5): e1002656. doi:10.1371/journal.ppat.1002656. PMC 3342959. PMID 22570609.
^Koelle K, Cobey S, Grenfell B, Pascual M (December 2006). "Epochal evolution shapes the phylodynamics of interpandemic influenza A (H3N2) in humans". Science. 314 (5807): 1898–903. Bibcode:2006Sci...314.1898K. doi:10.1126/science.1132745. PMID 17185596. S2CID 13873690.
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