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Characteristics of three strains of feline fibrosarcoma virus grown in cat and marmoset monkey cells
Author(s) -
McDonald Ruth,
Thakkar Bakul,
Wolfe Lauren G.,
Deinhardt Friedrich
Publication year - 1976
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.2910170317
Subject(s) - marmoset , fibrosarcoma , virology , biology , virus , callithrix , cats , pathology , medicine , genetics , paleontology
Two strains of feline fibrosarcoma virus (ST‐FeSV and GA‐FeSV) were found to induce tumors in cats and marmosets, and to transform feline and marmoset cells in vitro after primary inoculation. A third strain (SM‐FeSV) failed to induce tumors or transform marmoset cells after primary inoculation; however, when SM‐FeSV‐infected marmoset cultures were passed 26 times in vitro, the cell cultures released infectious virus which transformed marmoset fibroblasts but still failed to induce tumors in marmosets. ST‐FeSV induced mainly round‐cell type transformation (r foci), GA‐FeSV induced predominantly mixed round‐fusiform cell type transformation (fr foci), and SM‐FeSV induced r and fr type foci with a higher proportion of fusiform cells in the fr foci than seen with GA‐FeSV. Transforming virus was obtained from r or mixed r/fr foci of ST‐FeSV but not from fr foci; heat treatment changed the virus from producing almost exclusively r type foci to inducing an increased number of fr foci. Passage of FeSV in cat cells yielded viruses with a higher ratio of infectivity for feline vs marmoset cells, while passage of FeSV in marmoset cells yielded virus with a relatively higher infectivity ratio for marmoset cells; the three strains differed in the degree of change in the infectivity ratio. Despite the alteration of host range of SM‐FeSV propagated in marmoset fibroblasts, the virus retained feline P‐30 antigen by CF and FA assays. Neutralization tests did not indicate but also did not exclude an alteration of the surface antigens of ST‐FeSV or SM‐FeSV propagated in marmoset fibroblasts. The alteration of the relative infectivity of FeSV during passage in marmoset cells may be due to: (1) the selection of a variant present in the original heterogeneous uncloned population; (2) mutation; or (3) recombination with some marmoset genetic material, possibly an as yet unidentified endogenous marmoset virus.