Publication: FV‐2<sup>r</sup>‐mediated resistance of mouse bone‐marrow cells to friend spleen focus‐forming virus infection
Issued Date
1980-01-01
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ISSN
10970215
00207136
00207136
Other identifier(s)
2-s2.0-0018910899
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Mahidol University
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SCOPUS
Bibliographic Citation
International Journal of Cancer. Vol.26, No.1 (1980), 101-106
Suggested Citation
Chalobon Yoosook, Richard Steevesz, Frank Lilly FV‐2<sup>r</sup>‐mediated resistance of mouse bone‐marrow cells to friend spleen focus‐forming virus infection. International Journal of Cancer. Vol.26, No.1 (1980), 101-106. doi:10.1002/ijc.2910260116 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/11089
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Title
FV‐2<sup>r</sup>‐mediated resistance of mouse bone‐marrow cells to friend spleen focus‐forming virus infection
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Abstract
A target cell assay based on the formation of infectious centers (IC) was used to characterize the Fv‐2resistance gene of mice. Dose‐response curves were obtained for the number of IC generated from incubated mixtures of bone‐marrow cells and Friend virus (FV). The hemopoietic stimulus of bleeding increased the frequency of potential 〈target〉 cells capable of forming 1C in DBA/2 but not in D2.Fv‐2 r mice; however, even without the bleeding stimulus D2.Fv‐2 r mice contained fewer target cells in their bone marrow than DBA/2 mice. During the first 48 h postinfection a massive dose of FV overcame the inhibitory effect of the FV‐2 r gene as measured by the release of FV from the spleen. However, the concentration of 1C recoverable from the spleens of these infected mice was still much lower in the D2.Fv‐2 r strain. When irradiated F 1 hybrid hosts were used as recipients for the proliferation of infected donor cells, splenic 1C were not generated as efficiently from infected bone‐marrow cells of D2.Fv‐2 r origin as from those of DBA/2 origin. However, the amounts of SFFV recoverable were approximately the same. Similarly, after in vitro infection there was no great difference between the amounts of SFFV released from bonemarrow cells of DBA/2 and D2.Fv‐2 r mice. We conclude that the primary effect of the Fv‐2 r gene may be to inhibit the formation and proliferation of 1C in vivo, and that SFFV replication could be inhibited secondarily. Copyright © 1980 Wiley‐Liss, Inc., A Wiley Company