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. 1977 Dec;18(3):868–871. doi: 10.1128/iai.18.3.868-871.1977

Effect of input multiplicity on the establishment of simian virus 40 persistent infections in rhesus monkey kidney cells.

L C Norkin
PMCID: PMC421316  PMID: 201570

Abstract

Monolayer cultures of LLC-MK2 rhesus monkey kidney cells become persistently infected with simian virus 40 after infection at input multiplicities of 100, 10, or 1 plaque-forming unit per cell. After 3 weeks, all cells of the cultures infected at a multiplicity of 1 plaque-forming unit per cell produced the simian virus 40 T antigen. In contrast, 8 to 11 weeks elapsed before all the cells in the cultures infected at a multiplicity of 100 plaque-forming units per cell produced T antigen. Defective interfering particles and interferon production were not evident during this time.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Hahn E. C., Sauer G. Initial stage of transformation of permissive cells by simian virus 40: development of resistance to productive infection. J Virol. 1971 Jul;8(1):7–16. doi: 10.1128/jvi.8.1.7-16.1971. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Hahn E. C. The development of CV-1 cells resistant to SV 40. Arch Gesamte Virusforsch. 1972;37(1):34–44. doi: 10.1007/BF01241148. [DOI] [PubMed] [Google Scholar]
  3. Huang A. S., Baltimore D. Defective viral particles and viral disease processes. Nature. 1970 Apr 25;226(5243):325–327. doi: 10.1038/226325a0. [DOI] [PubMed] [Google Scholar]
  4. Lombardi P. S., Balduzzi P., Hare J. D., Morgan H. R. Mechanism of the development of a stable carrier system of L cells with polyoma virus. J Natl Cancer Inst. 1970 Jul;45(1):171–178. [PubMed] [Google Scholar]
  5. Norkin L. C., Ouellette J. Cell killing by simian virus 40: variation in the pattern of lysosomal enzyme release, cellular enzyme release, and cell death during productive infection of normal and simian virus 40-transformed simian cell lines. J Virol. 1976 Apr;18(1):48–57. doi: 10.1128/jvi.18.1.48-57.1976. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Norkin L. C. Rhesus monkeys kidney cells persistently infected with Simian Virus 40: production of defective interfering virus and acquisition of the transformed phenotype. Infect Immun. 1976 Sep;14(3):783–792. doi: 10.1128/iai.14.3.783-792.1976. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Preble O. T., Youngner J. S. Temperature-sensitive viruses and the etiology of chronic and inapparent infections. J Infect Dis. 1975 Apr;131(4):467–473. doi: 10.1093/infdis/131.4.467. [DOI] [PubMed] [Google Scholar]
  8. Rima R. K., Martin S. J. Persistent infection of tissue culture cells by RNA viruses. Med Microbiol Immunol. 1976 Jun 1;162(2):89–119. doi: 10.1007/BF02121320. [DOI] [PubMed] [Google Scholar]
  9. SWEET B. H., HILLEMAN M. R. The vacuolating virus, S.V. 40. Proc Soc Exp Biol Med. 1960 Nov;105:420–427. doi: 10.3181/00379727-105-26128. [DOI] [PubMed] [Google Scholar]
  10. Wilson J. H., DePamphilis M., Berg P. Simian virus 40-permissive cell interactions: selection and characterization of spontaneously arising monkey cells that are resistant to simian virus 40 infection. J Virol. 1976 Nov;20(2):391–399. doi: 10.1128/jvi.20.2.391-399.1976. [DOI] [PMC free article] [PubMed] [Google Scholar]

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