Role of the Host Cell in Persistent Viral Infection: Coevolution of L Cells and Reovoirus During Persistent Infection

Cell. 1981 Aug;25(2):325-32. doi: 10.1016/0092-8674(81)90050-7.

Abstract

Mutant L cells, designated LR cells, were isolated after "curing" a persistently infected cell line (L/C) with antireovirus serum. The LR cells were shown to be virus-free; no reovirus was detectable by infectious center assays, plaque assays, presence of viral proteins, presence of viral dsRNA and immunofluorescence studies. Persistent infections were readily established n LR cells following infection with either cloned, low passage wild-type reovirus or cloned, low passage reovirus isolated from carrier cultures. Reovirus isolated from carrier cultures, however, grew much better than wild-type reovirus in LR cells and showed complete dominance over wild-type reovirus in coinfection experiments. Infection of LR cells with wild-type reovirus resulted in a low-level persistent infection with inefficient viral replication; these mutant L cells were partially resistant to infection with wild-type reovirus. In contrast, infection of the mutant L cells with virus isolated from the persistently infected cells resulted in a persistent infection accompanied with efficient viral replication. Infection of the original L cells with either wild-type reovirus or reovirus isolated from the persistently infected cells resulted in a lytic infection with no surviving cells. Thus the host cell plays a crucial role in the maintenance of persistent reovirus infection. Our results show that there is a coevolution of both mutant L cells and mutant reovirus during persistent infection.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Clone Cells
  • Cytopathogenic Effect, Viral
  • L Cells / microbiology*
  • Mammalian orthoreovirus 3 / genetics
  • Mammalian orthoreovirus 3 / growth & development*
  • Mice
  • Mutation
  • Reoviridae / genetics
  • Reoviridae / growth & development*
  • Virus Replication