Abstract
Reassortments and point mutations are two major contributors to diversity of Influenza A virus; however, the link between these two processes is unclear. It has been suggested that reassortments provoke a temporary increase in the rate of amino acid changes as the viral proteins adapt to new genetic environment, but this phenomenon has not been studied systematically. Here, we use a phylogenetic approach to infer the reassortment events between the 8 segments of influenza A H3N2 virus since its emergence in humans in 1968. We then study the amino acid replacements that occurred in genes encoded in each segment subsequent to reassortments. In five out of eight genes (NA, M1, HA, PB1 and NS1), the reassortment events led to a transient increase in the rate of amino acid replacements on the descendant phylogenetic branches. In NA and HA, the replacements following reassortments were enriched with parallel and/or reversing replacements; in contrast, the replacements at sites responsible for differences between antigenic clusters (in HA) and at sites under positive selection (in NA) were underrepresented among them. Post-reassortment adaptive walks contribute to adaptive evolution in Influenza A: in NA, an average reassortment event causes at least 2.1 amino acid replacements in a reassorted gene, with, on average, 0.43 amino acid replacements per evolving post-reassortment lineage; and at least ∼9% of all amino acid replacements are provoked by reassortments.
Highlights
The genome of influenza A virus consists of 8 segments, each represented by an RNA molecule
Assuming that an incongruence between phylogenies of two segments, observed in a high fraction of comparisons, reflects an ancestral reassortment event, GiRaF predicts the subsets of taxa that are descendant to such reassortments
When the histories of reassortment events are complex, the subsets of genotypes resulting from a single reassortment predicted by GiRaF are not necessarily monophyletic [12]
Summary
The genome of influenza A virus consists of 8 segments, each represented by an RNA molecule. Most of the major Influenza A pandemics during the last century were caused by reassortant strains [1]. Reassortments, especially those creating novel combinations of hemagglutinin (HA) and neuraminidase (NA) genes, may lead to radical changes in antigenic properties and give rise to viral types that escape the herd immunity. It is likely that only a small proportion of reassortment events lead to creation of novel, successful viral genotypes. Reassortments between different Influenza A subtypes gave rise to the major pandemics of the 1957, 1968, 2009, and possibly 1918 [1,4]. Reassortments between strains belonging to a single subtype likely occur much more frequently than inter-subtype reassortments; they leave a less pronounced phylogenetic signal, and are harder to study [5]
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