Defective interfering particles in mice infected with lymphocytic choriomengingitis virus

Continuous cultivation of murine L cells infected with lymphocytic choriomeningitis virus strain Armstrong leads to production of L(Arm) cells, which produce a predominantly cell-associated attenuated variant, the L(Arm) virus. The relatively few infectious particles that are released have lost the ability to form plaques on L cells and to cause illness in mice even if inoculated intracerebrally. Based on equal protein MrS, antigenicity and protein kinase activity, essentially identical results were obtained for the purified Armstrong and L(Arm) viruses. There was also no difference in production and release of particles with the potential to cause homologous interference. Such particles consisted of two types, one of which was highly susceptible to u.v.-irradiation, the other was highly resistant. In the case of the L(Arm) virus interfering particles, it appears that the u.v.-irradiation-susceptible forms represented infectious virus. Purified L(Arm) virus particles contained considerable quantities of subgenomic forms of (small) S-and (large) L-RNA and their complementary counterparts, which all appeared to be replicated autonomously in an unenriched manner.

Section: Discussionmentioning

confidence: 99%

Characterization of a virus variant produced by L cells persistently infected with lymphocytic choriomeningitis virus

Stöcker

Peralta²,

Kratzberg³

et al. 1994

“…Persistent infections are characterized by reduced viral replication, limited accumulation of viral glycoproteins at the surface of infected cells and the generation of LCMV-specific interfering particles that appear very rapidly after initiation of infection (Buchmeier et al, 1980;Lehmann-Grube et al, 1980;Oldstone & Buchmeier, 1982;Popescu & Lehmann-Grube, 1977;Welsh & Buchmeier, 1979). The net result is a significant reduction in the production of infectious particles.…”

Section: Introductionmentioning

confidence: 99%

Deleted Viral RNAs and Lymphocytic Choriomeningitis Virus Persistence in vitro

Francis

Southern

1988

SUMMARYLymphocytic choriomeningitis virus (LCMV) infection of most tissue culture cell lines results in a non-cytopathic persistent infection. Persistent infections in vitro share many characteristics with persistent LCMV infection of mice; both are associated with decreased titres of infectious virus, restricted accumulation of viral glycoproteins at the surface of infected cells and the generation of interfering particles. We have used gel electrophoresis and hybridization techniques to analyse LCMV gene expression during persistent infection of a number of tissue culture cell lines. Our study has demonstrated that, although deleted viral RNAs can be detected during persistent LCMV infection in vitro, there may not be an obligatory association between deleted RNAs and persistence. In addition, we have found that LCMV interfering activity can be produced in the apparent absence of deleted intracellular viral RNAs.

“…Since then a large literature has accumulated showing that in cultured cells DI particles modulate acute virus infections and are involved in the establishment and/or maintenance of persistent infections Perrault, 1981) including infection with Semliki Forest virus (SFV) (Stark & Kennedy, 1978). However, there have been relatively few reports on the effects of DI viruses on acute infections of animals (Barrett & Dimmock, 1984a, b, c;Barrett et al, 1984b;Crouch et al, 1982;Dimmock & Kennedy, 1978;Doyle & Holland, 1973;Fultz et al, 1982a;Mims, 1956;Popescu & Lehmann-Grube, 1977;Rabinowitz et al, 1977;Rabinowitz & Huprikar, 1979;Spandidos & Graham, 1976;von Magnus, 1951 ;Welsh et al, 1977) and much of the earlier work is difficult to interpret as it lacked controls to exclude immunogenic effects of DI virus. The involvement of DI viruses in persistent infections of animals has not been established with any certainty.…”

Section: Persistence Of Virulent Semliki Forest Virus In Mouse Brain mentioning

confidence: 99%

Persistence of Virulent Semliki Forest Virus in Mouse Brain Following Co-inoculation with Defective Interfering Particles

Atkinson

Barrett

Mackenzie

et al. 1986

SUMMARYSemliki Forest virus (SFV) normally causes an acute lethal encephalitis in mice following intranasal inoculation. However, animals co-administered with 10 LDso SFV and defective interfering (DI) SFV survive the infection without clinical signs of disease. In this report we demonstrate the isolation of infectious virus from the brains of 12/169 protected mice up to 6-5 months post-infection. Although, with one exception, mice were clinically normal, five of 12 of the SFV isolates were identical to the original virus as judged by plaque morphology, maximum temperature for growth, virulence in mice and pathology. Others were less virulent (although not any were plaque or temperature-sensitive mutants) and on re-inoculation into fresh mice caused a demyelinating pathology which was not an attribute of the original inoculum. How the virulent virus can persist in brain, sometimes in amounts in excess of 100 LDso, without causing disease remains to be determined.