Evolution of a Coronavirus during Persistent Infection in Vitro

Holmes, Kathryn V.; Behnke, James

doi:10.1007/978-1-4757-0456-3_23

Cited by 47 publications

(47 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Coronavirions are subject to an intracellular postbudding maturation process that occurs while they are on their way through the constitutive exocytic pathway by which they are exported out of the cell (Risco et al, 1998;Salanueva et al, 1999;Tooze et al, 1987). Indications of this had already been noticed in early morphological studies with HCoV-229E (Becker et al, 1967;Chasey and Alexander, 1976;Hamre et al, 1967;Oshiro et al, 1971) and MHV (Holmes and Behnke, 1981;, but were described in somewhat more detail for MHV by Tooze and coworkers (1987). The pictures show "immature" virions in pre-Golgi compartments and Golgi cisternae that appear as spherical structures with the ribonucleoprotein core immediately below the viral envelope and with an "empty" center.…”

Section: B Postassembly Maturation Of Virionsmentioning

confidence: 93%

Molecular Interactions in the Assembly of Coronaviruses

Haan

Rottier

2005

Advances in Virus Research

357

348

View full text Add to dashboard Cite

Section: B Postassembly Maturation Of Virionsmentioning

confidence: 93%

Molecular Interactions in the Assembly of Coronaviruses

Haan

Rottier

2005

Advances in Virus Research

357

348

View full text Add to dashboard Cite

“…In recent years members of the murine coronaviruses have been studied extensively because of their ability to establish persistent infections both in vitro (Holmes & Behnke, 1981 ;Stohlman & Weiner, 1978;Lucas et al, 1977Lucas et al, , 1978Leibowitz et al, 1984;Lamontagne & Dupuy, 1984) and in vivo (Knobler et al, 1981;Hirano et al, 1980;Nagashima et al, 1979;Sorensen et al, 1980Sorensen et al, , 1982Sorensen et al, , 1984. Because of this property, these agents have been considered as useful models for several chronic disease states including demyelinating diseases.…”

Section: Introductionmentioning

confidence: 99%

“…The mechanisms that allow these coronaviruses to be maintained in a persistent manner are not clear at present. It is apparent that mechanisms involving such factors as interferon, temperature-sensitive viral mutants and defective interfering viral particles, which are common for other viral agents that persist, are not operating for a majority of persistent coronavirus infections (Lucas et al, 1977(Lucas et al, , 1978Stohlman & Weiner, 1978 ;Leibowitz et al, 1984;CoulterMackie et al, 1985), although in some cases mutant viruses have been identified (Stohlman et al, 1979;Holmes & Behnke, 1981). Thus it appears that the type of host cell is a major determinant in the persistent replication of these agents.…”

Section: Introductionmentioning

confidence: 99%

Several Rat Cell Lines Share a Common Defect in Their Inability to Internalize Murine Coronaviruses Efficiently

Flintoff¹,

Dinter²

1989

Journal of General Virology

View full text Add to dashboard Cite

SUMMARYInfection of rat cells, Schwannoma RN2, hepatoma HTC or myoblast L6, with the murine coronavirus JHM strain results in a persistent infection characterized by the release of virus over an extended period of time with a limited cytopathology. Several stages of the viral replication cycle have been examined in these cells in comparison to those in mouse L2 cells, which are totally permissive to JHM infection. Although the rat cells bound as much virus as the mouse cells their ability to internalize it was 40-fold less efficient than the mouse cells. This lower internalization efficiency was not enhanced by pH shock of infected cells, but was by treatment with polyethylene glycol. In all cell types there appeared to be no major differences in the ability of the internalized virus to replicate the viral RNA as determined by slot-blot analysis with a radiolabelled viral cDNA. A similar genetic mechanism appears to be operative in the lines because somatic cell hybrids formed between these lines in various combinations were also deficient in the ability to internalize bound virus. Taken together these results imply that rat cell lines in general share a common deficiency in their inability to internalize murine coronaviruses efficiently. This low efficiency in viral internalization may explain in part the ability of these lines to sustain persistent infections.

show abstract

“…Nevertheless, the mechanisms by which the outcome of such infection is determined remain poorly understood. Studies in cell culture have implicated the involvement of attenuated MHV variants such as heat-sensitive (Holmes & Behnke, 1981), cold-sensitive (Stohlman et al, 1979) and small plaque (Hirano et al, 1981) mutants. Evidence from in vivo studies has also been presented suggesting the generation during long-term nervous system infection of virus variants which give rise to altered mRNAs (Jackson et al, 1984;Taguchi et al, 1987).…”

mentioning

confidence: 99%

A Model for Persistent Murine Coronavirus Infection Involving Maintenance via Cytopathically Infected Cell Centres

Macintyre¹,

Wong²,

Anderson³

1989

Journal of General Virology

View full text Add to dashboard Cite

SUMMARYThe relatively cell impermeable hygromycin B was found to inhibit viral but not cellular protein synthesis when added to cultures of murine hepatitis virus (MHV)-infected or mock-infected mouse L-2 fibroblasts. Membrane permeability, as judged by influx of sodium ions, has previously been demonstrated to be an MHV E2 glycoprotein-mediated, cytopathic effect of MHV infection in L-2 cells. It is therefore likely that the selective effect of hygromycin B on viral protein synthesis is a reflection of an increased drug penetration into virus-infected cells. Using hygromycin B as a marker for MHV-indueed cell membrane cytopathology, the effects of drug treatment on a persistent MHV infection in mouse LM-K fibroblasts were investigated. MHV persistence in LM-K cells, which normally involves a steady state infection of 0.1 to 1% of the cells in culture, was found to be cured by hygromycin B treatment, as measured by the elimination of infectious virus from the supernatant medium. Hygromycin B also resulted in the eradication of MHV-specific RNA from LM-K cells, arguing against the presence of a non-cytopathically or latently infected subpopulation of cells.

show abstract

Evolution of a Coronavirus during Persistent Infection in Vitro

Cited by 47 publications

References 7 publications

Molecular Interactions in the Assembly of Coronaviruses

Molecular Interactions in the Assembly of Coronaviruses

Several Rat Cell Lines Share a Common Defect in Their Inability to Internalize Murine Coronaviruses Efficiently

A Model for Persistent Murine Coronavirus Infection Involving Maintenance via Cytopathically Infected Cell Centres

Contact Info

Product

Resources

About