The influenza C virus belongs to the
Orthomyxoviridae family and is a common cause of mild upper respiratory tract illness. Seroepidemiological studies indicate that it is widely distributed around the world, but isolated infrequently, and the majority of humans acquire antibodies to the virus early in life [
1]. In contrast with influenza A and B viruses, the influenza C virus genome consists of only seven single stranded negative-sense RNA segments, the PB2, PB1, P3, HE, NP, M, and NS segments. Analysis of the full genome sequence of type C influenza viruses suggested that reassortment between two different type C influenza viruses occurs frequently in nature [
2,
3]. Furthermore, influenza C virus has been suggested to be involved in heterologous RNA recombination events [
4].
Largely because their RNA is always encapsidated by a ribonucleoprotein complex (RNP), single-stranded negative-sense RNA viruses are generally believed to undergo a low rate of homologous recombination [
5]. However, there is increasing evidence of homologous recombination involving negative-strand RNA viruses like Newcastle disease virus [
5‐
8], Zaire Ebola virus [
9], measles virus [
10], and canine distemper virus [
11,
12]. Homologous recombination has also been demonstrated in the laboratory for respiratory syncytial virus and hantavirus [
13,
14]. However, the evidence for homologous recombination in influenza viruses has been sparse and controversial. Gibbs et al. proposed that homologous recombination had occurred in the HA gene of 1918 Spanish flu virus [
15]. However, the apparent recombination event described by Gibbs et al. is much more likely the result of a difference in the substitution rate between HA1 and HA2 [
16]. Several recent studies provide some new evidence for recombination in influenza A virus [
17‐
19]. In particular, He et al. provide evidence for a clade of three recombinant avian influenza sequences [
17], but large-scale analyses have shown that anomalies in the influenza sequence database, possibly caused by sample contamination, may generate false-positive recombination signals [
20‐
22]. Indeed, when controlling for sequence quality, the evidence for homologous recombination is weak in both influenza A and B viruses [
20,
22,
23]. Given the evidence to date, homologous recombination seems to play little or no role in the evolution of influenza A and B viruses. In a previous small scale analysis, patterns of sequence variation compatible with the action of recombination, but not definitive evidence, were observed in influenza C virus [
5]. The increasing availability of genome sequences of influenza C virus may have the potential to shed new light on the role of homologous recombination in the evolution of influenza C virus.