Secondary infection with rescued M-MSV is requisite for focus formation of S+L- mink cells by murine leukemia virus.
Whether the foci on S+L- mink cells transformed by the superinfection of MuLV were induced by the secondary infection of M-MSV pseudotype generated in the cells or by the secondary infection of MuLV has remained unresolved since the requirement of secondary infection was first reported (A. Ishimoto, J. Virol. 36, 18-21, 1980). Here, we show that infection with ecotropic MuLV of S+L- mink cells transfected with the receptor gene for ecotropic MuLV induced transformed foci resembling those induced by xenotropic and amphotropic viruses. This observation and our previous results (A. Ishimoto, J. Virol. 36, 18-21, 1980) that clonal lines of S+L- mink cells chronically infected with ecotropic MuLV are morphologically indistinguishable from normal S+L- mink cells suggest that the focus formation of S+L- mink cells by superinfection with MuLV is not due to secondary spread of helper virus which transactivates the expression of the v-mos oncogene by the MuLV, but is due to the secondary infection of the defective M-MSV genome. A new S+L- mink cell line with a receptor gene for ecotropic MuLV, designated ID cells, provided a new method for titrating the ecotropic MuLV that develop few XC foci and to simultaneously detect viruses in various host ranges.
Wang
L
L
Department of Viral Oncology, Kyoto University, Japan.
Hirama
T
T
Higo
K
K
Nakagawa
Y
Y
Kubo
Y
Y
Kobayashi
H
H
Kakimi
K
K
Ishimoto
A
A
D000818:Animals; D002472:Cell Transformation, Viral / Q000502:physiology*; D002478:Cells, Cultured; D008907:Mink / Q000382:microbiology*; D008908:Mink Cell Focus-Inducing Viruses / Q000502:physiology*; D008980:Moloney murine sarcoma virus / Q000502:physiology*