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The interaction of polyoma virus with F9 embryonal carcinoma cells and chemically induced differentiated progeny: Fate of the viral DNA and expression of viral antigens
Author(s) -
Trevor Katrina,
Lehman John M.
Publication year - 1982
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041130512
Subject(s) - biology , embryonal carcinoma , cell culture , virus , retinoic acid , cellular differentiation , microbiology and biotechnology , antigen , viral replication , virology , gene , immunology , biochemistry , genetics
Murine embryonal carcinoma (EC) cells fail to express viral T antigen following infection with polyoma (Py) virus, while some differentiated derivatives are fully susceptible to viral infection. The block to expression in EC cells apparently occurs after adsorption and penetration but prior to the synthesis of early viral proteins. The F9 EC cell line was employed to further investigate the failure of Py gene expression in EC cells as well as the viral susceptibility of certain differentiated cell types. F9 cultures treated with retinoic acid (RA) or RA in combination with dibutyryl cAMP (dBcAMP) are quantitatively induced to differentiate to endodermal cell types. When the fate of the viral DNA was examined in F9 EC cells, free viral DNA was observed early after infection but was eventually lost with continued cell growth. Cultures induced to differentiate in the presence of RA demonstrated limited viral susceptibility which increased with prolonged RA exposure. Polyoma sensitivity did not directly parallel basement membrane antigen production, a marker used to distinguish this differentiated endodermal cell type. Viral gene expression could be obtained if Py DNA was introduced into the cells prior to RA induction. In contrast, the endodermal progeny derived from a dual treatment with RA plus dBcAMP appeared highly refractory to Py infection.