title: Persistent infection with an influenza C virus variant is dominantly established in the presence of the parental wild-type virus.
abstract: Two influenza C viruses were used for double-infection experiments to investigate the dominance of their phenotypes. The wild-type virus (C/AA-wt) had been characterized by its short-lived productive cycle, whereas a distinct variant derived from it (C/AA-pi) was demonstrated to persist in long-term passages of infected MDCK cultures. Here we show that the persistent virus C/AA-pi is capable of replicating in the presence of abundant amounts of wild-type virus: the persistent virus could be diluted to 10(-9) within wild-type inoculum, still developing a stable form of persistence. This behaviour was reflected by permanent virus release and by continuous enzymatic activity of the viral HEF glycoprotein in infected cells. All long-term cultures tested remained positive for viral NS protein and vRNA. On the vRNA level, it was shown that viral segments originated from the persistent-type genome, while wild-type vRNAs were not maintained after double-infection. Thus, the genotype of the persistent variant was dominantly selected in serial passages. These results indicate a specific intracellular advantage of persistent influenza C virus over the parental wild-type.
authors.affiliation: Abteilung für Virologie, Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, Germany. tbl1101@mail.lrz-muenchen.de
authors.forename: M
authors.initials: M
authors.lastname: Marschall
authors.forename: A
authors.initials: A
authors.lastname: Helten
authors.forename: A
authors.initials: A
authors.lastname: Hechtfischer
authors.forename: A
authors.initials: A
authors.lastname: Zach
authors.forename: H
authors.initials: H
authors.lastname: Meier-Ewert
mesh_terms: D000818:Animals; D002460:Cell Line; D002642:Chick Embryo; D004285:Dogs; D014644:Genetic Variation; D006801:Humans; D009982:Gammainfluenzavirus / Q000235:genetics / Q000502:physiology*; D017735:Virus Latency