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Further studies on mouse sarcoma virus (moloney) replication in human cells. Partial host range shift of progeny virus
Author(s) -
Bernard C.,
Chuat J. C.,
Laprevotte I.,
Boiron M.
Publication year - 1972
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910100310
Subject(s) - tropism , biology , virus , virology , multiplicity of infection , viral replication , tissue tropism , cell culture , viral transformation , in vivo , transformation (genetics) , in vitro , genetics , gene
Several human cell lines were examined for their susceptibility to infection by mouse sarcoma virus, strain Moloney (M‐MSV). Successful transformation was achieved only with concentrated virus from rat cell line 78 Al. The lag time and the extent of cellular alteration were found to be related to the employed multiplicity of infection (total transformation within 4 days at a multiplicity of 0.1). All the experiments performed showed the tropism of the progeny virus (HU‐MSV) to shift from a double murine and human tropism to exclusive human tropism as far as the transforming function is concerned. On the contrary, nontransforming replication in mouse cells was continuously obtained. In vivo studies yielded parallel results: only the leukemogenic potential of HU‐MSV for mice was found to persist. The mechanism of this dissociated host‐range shift of transforming and non‐transforming virions is discussed.