Studies of L Cells Persistently Infected with VSV: Factors Involved in the Regulation of Persistent Infection
- 1 May 1977
- journal article
- research article
- Published by Microbiology Society in Journal of General Virology
- Vol. 35 (2) , 265-279
- https://doi.org/10.1099/0022-1317-35-2-265
Abstract
Summary Infection of interferon-treated L cells with VSV led frequently to the establishment of L cells persistently infected with VSV (Lvsv cells). These cells were characterized by the following properties; (1) no supplement of antiviral factors such as anti-VSV antiserum, interferon, was required for their maintenance; (2) virus antigens were detected in about 5 to 30% of the cells by immunofluorescence staining; (3) the cells were not only resistant to superinfection by homologous virus, but also resistant to challenge by heterologous viruses such as Mengo virus; (4) the cells were destroyed by co-cultivation with heterologous cells susceptible to VSV infection; (5) the cells could be cured by serial cultivation in medium containing antiviral antibody, and the cured cells were as susceptible to VSV as normal L cells. It was shown that at least three factors (interferon, defective interfering [DI] particles and a selection of small-plaque temperature-sensitive [ts] mutants) took part in the maintenance of Lvsv cells although it was difficult to evaluate exactly the relative importance of these factors. The effect of antiviral antibody, interferon and incubation temperature upon the maintenance of Lvsv cells are discussed further.This publication has 4 references indexed in Scilit:
- Polykaryocyte Formation Induced by VSV in Mouse L CellsJournal of General Virology, 1976
- Relationship between Establishment of Persistent Infection of Haemagglutinating Virus of Japan and the Properties of the VirusJournal of General Virology, 1976
- Biologic Properties of Two Plaque Variants of Vesicular Stomatitis Virus (Indiana Serotype)The Journal of Immunology, 1963
- Virus-cell relationship in a carrier culture of HeLa cells and Coxsackie A9 virusVirology, 1959