A Variant Schmidt‐Ruppin Strain of Rous Sarcoma Virus with Increased Affinity for Mammalian Cells

• Published in: Cancer science 1989-12, Vol.80 (12), p.1179-1185
• Main Authors: Kawai, Sadaaki, Nishizawa, Makoto, Shinno‐Kohno, Hideko, Shiroki, Kazuko
• Format: Article
• Language: English
• Subjects: Adenovirus E1A gene; Affinity; AIDS/HIV; Amphotericin B; Amphotericin B - pharmacology; Animals; Avian Sarcoma Viruses - genetics; Avian Sarcoma Viruses - isolation & purification; Avian Sarcoma Viruses - pathogenicity; Avian Sarcoma Viruses - physiology; Biological and medical sciences; Cell fusion; Cell Transformation, Viral - drug effects; Cells, Cultured; Chick Embryo; Cricetinae; E1A protein; Efficiency; Env gene; Envelope glycoprotein; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Products, env - genetics; Genetic transformation; Mammalian cells; Mammalian tropism; Microbiology; Mutation; Rats; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Rous sarcoma virus; Tropism; Viral Plaque Assay; Virology
• ISSN: 0910-5050; 1347-9032; 1349-7006; 1876-4673
• DOI: 10.1111/j.1349-7006.1989.tb01652.x

SR‐RSV‐D(H), a variant virus with extremely high tropism for mammalian cells, was isolated by passage of the Schmidt‐Ruppin strain of Rous sarcoma virus of subgroup D (SR‐RSV‐D) through hamster cells. This variant virus has acquired an altered envelope glycoprotein, encoded by the env gene, that has high affinity for receptors on the surface of mammalian cells. The variant virus transforms rat cells at about 100 times the efficiency of the parental virus, SR‐RSV‐D(S), as assayed by focus formation. Addition of amphotericin B (Fungizone) to the medium at a concentration of 0.2 μg/ml completely inhibited rat cell transformation by SR‐RSV‐D(H), possibly by blocking virus penetration into the cells, whereas the drug showed no inhibitory effect on transformation of chick embryo flbroblast (CEF) cells by the variant virus or on transformation of rat cells by the parental virus. The efficiency of transformation of rat cells by the variant virus was much less than its efficiency of transformation of CEF cells. Analysis of infection of rat cells suggested that the virus can infect rat cells as efficiently as CEF cells but that rat cells were not transformed by the virus as fully as CEF cells because of inefficiency of some post‐penetrational step involved in viral gene expression. The finding that El AY cells, rat cells expressing adenovirus El A gene, were transformed by SR‐RSV‐D(H) as efficiently as CEF cells supports this conclusion and suggests that expression of the E1A gene in rat cells may overcome the defect in the transforming step(s) in rat cells.