Genetic resistance to Rous sarcoma virus in embryo cell cultures and embryos

Crittenden, L. B.; Okazaki, W.; Reamer, R. H.

doi:10.1016/0042-6822(63)90107-7

Cited by 44 publications

(9 citation statements)

References 2 publications

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“…Similar results were found in a different set of highly inbred lines of chickens in which RSV was applied on the CAM of chicken embryos or in cell culture and measured respectively by pocks on the CAM and/or transformed foci, as well as virus production by cell cultures (67). It had previously been shown that these assay methods gave the same results as tumor production after inoculation into hatched chickens (68).…”

Section: Genetics Of Susceptibility and Resistance Tomentioning

confidence: 95%

The early history of tumor virology: Rous, RIF, and RAV

Rubin

2011

Proc. Natl. Acad. Sci. U.S.A.

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One hundred years ago Peyton Rous recovered a virus, now known as the Rous sarcoma virus (RSV), from a chicken sarcoma, which reproduced all aspects of the tumor on injection into closely related chickens. There followed recovery of causal viruses of tumors of different morphology from 4 more of 60 chicken tumors. Subsequent studies in chickens of the biology of the first RSV isolated moved slowly for 45 y until an assay of ectodermal pocks of the chorioallantoic membrane of chicken embryos was introduced. The inadequacies of that assay were resolved with the production of transformed foci in cultures of chicken fibroblasts. There followed a productive period on the dynamics of RSV infection. An avian leukosis virus (ALV) was found in some chicken embryos and named resistance-inducing factor (RIF) because it interferes with RSV. Its epidemiology in chickens is described. Another ALV was found in stocks of RSV and called Rous-associated virus (RAV). Cells preinfected with RAV interfere with RSV infection, but RSV does not produce infectious virus unless RAV is added during or after RSV infection. Intracellular RAV provides the infectious coat for the otherwise defective RSV. The coat determines the antigenicity, host range, and maturation rate of RSV. RSV particles carry reverse transcriptase, an enzyme that converts their RNA into DNA and allows integration into the cell's DNA, where it functions as a cellular gene. This was the bridge that joined the biological era to the molecular era. Its relation to oncogenes and human cancer is discussed.

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Section: Genetics Of Susceptibility and Resistance Tomentioning

confidence: 95%

The early history of tumor virology: Rous, RIF, and RAV

Rubin

2011

Proc. Natl. Acad. Sci. U.S.A.

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“…This is in agreement with work published by Bower et al (1965). Crittenden et al (1963) have reported that genetic resistance to Rous sarcoma virus is manifested by embryonic chick cells cultured in vitro.…”

Section: Discussionmentioning

confidence: 98%

Neutralizing Ability of Sera from Three Strains of Chickens for Rous Sarcoma Virus

1966

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“…The cellular genetic control of resistance and susceptibility to avian sarcoma and leukosis virus subgroups is exerted through three autosomal loci termed tva, tvb, and tvc, which affect the cellular response to viruses of subgroups A, B, and C, respectively. Tvb also influences the response to subgroups D and E. In each of these loci, susceptibility is dominant over resistance, suggesting that they code for cellular receptors which may specifically mediate penetration for each of the subgroups (Crittenden et at., 1963(Crittenden et at., , 1964(Crittenden et at., , 1967Payne andBiggs, 1964, 1970;Rubin, 1965). The loci controlling resistance and susceptibility to host range subgroups A and C, tva and tvc, are linked to each other, but neither is linked to the locus for subgroup B, tvb .…”

Section: A Specific Interaction Between Envelope Glycoprotein and Celmentioning

confidence: 98%