## Abstract Virus induction in heterokaryons formed by non‐permissive cells transformed by Rous sarcoma virus (RSV) and permissive chick embryo (CE) cells, in the presence of inactivated Sendai virus, was studied with a clone of hamster BHK21 fibroblasts transformed by Schmidt‐Ruppin strain RSV (cl
Persistence of rous sarcoma virus in transformed non-permissive cells: mechanism of virus induction by association with permissive cells in the absence of sendai virus
✍ Scribed by Philippe Vigier
- Publisher
- John Wiley and Sons
- Year
- 1972
- Tongue
- French
- Weight
- 902 KB
- Volume
- 9
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
Virus induction by association of non‐permissive cells transformed by Rous sarcoma virus (RSV) and permissive chicken cells in the absence of Sendai virus has been studied with two clones of BHK21 hamster fibroblasts transformed respectively by Schmidt‐Ruppin strain RSV (clone RS2) and Bryan strain RSV (clone RB12), and with sub‐clones derived from these clones after many divisions. The main results have been the following: (1) All the transformed non‐permissive (TNP) cells presumably carry at least one complete viral genome since RSV could be recovered from all the subclones tested. (2) The first infective centers which appear in mixed cultures are presumably heterokaryons formed by spontaneous fusion of single TNP cells with chicken cells; and Rous cells (transformed chicken cells) which appear later on, arise by secondary infection of chicken cells. (3) The incidence of appearance of infective centers is low and can vary considerably depending on subclones in the case of RS2 cells. In the most highly inducible subclones, it never exceeds one center per 10^3^ RS2 cells and it can be much less in other subclones. (4) No induction was observed with two RS2 subclones from which RSV was nevertheless recovered after Sendai virus‐mediated cell fusion. (5) In the case of one of these subclones, even heterokaryon formation was inefficient in removing the block of virus production in the TNP cells. (6) No induction was obtained by any other method than cell association and no subviral determinant able to give rise to virus in CE cells was recovered from TNP cells.
The reasons for non‐permissiveness and the mechanism of induction are discussed.
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