## Abstract The host‐virus interactions of Simian virus 40 (SV^40^) and polyoma virus (Py) with cell lines established from a teratocarcinoma were studied. The cells utilized in this study were the multipotential stem cell of the teratocarcinoma, embryonal carcinoma, and differentiated cells derive
Temperature dependent expression of polyoma virus in murine embryonal carcinoma cells
✍ Scribed by L. Dandolo; M. Vasseur; C. Kress; J. Aghion; D. Blangy
- Publisher
- John Wiley and Sons
- Year
- 1980
- Tongue
- English
- Weight
- 639 KB
- Volume
- 105
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
At 37°C, undifferentiated murine teratocarcinoma cells (PCC4) are resistant to infection with SV40 and Polyoma virus. When infection is carried out at 31°C, these cells become fully susceptible to a variety of polyoma virus strains, including wt, ts‐a, and hr‐t; they also display an increased susceptibility to polyoma virus mutants (PyE.C.) which have been selected for their ability to develop in PCC4 cells at 37°C (Vasseur et al., '80). However, expression of SV40 is still restricted at 31°C and no T antigen can be detected. PCC4 cells grown at 31°C express the characteristic embryonal surface antigen(s), but no H2 antigen, and do not produce plasminogen activator.
PyE.C. mutants and other polyoma virus strains cannot develop at 37°C in nullipotent F9 embryonal carcinoma cells and restriction is not abolished at 31°C.
The results indicate that: (i) Resistance of PCC4 cells to polyoma virus and to SV40 are not mediated by the same process; (ii) loss of restriction of polyoma in PCC4 cells does not require cell differentiation; (iii) F9 and PCC4 cells control polyoma virus expression through different mechanisms.
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