Chromosome Abnormalities in vitro in Human Leukocytes Associated with Schmidt-Ruppin Rous Sarcoma Virus

Nichols, Warren W.; Levan, Albert; Coriell, Lewis L.; Goldner, Herman; Ahlström, C. G.

doi:10.1126/science.146.3641.248

Cited by 42 publications

(6 citation statements)

References 6 publications

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“…Chromosome breakage varied froni 10-30 percent, and again, the incidence of chromatid rearrangements was very low. 8 Similar results have been obtained in human leukocyte cultures in recent experiments using the oncogenic adenovirus-12 (FIGURE 1 ). Interestingly enough, the nononcogenic adenovirus-2 does not seem to have the capacity of producing breaks in leukocyte cultures, as can be seen in TABLE 1.…”

Section: Single Breakssupporting

confidence: 85%

Virus‐induced Chromosome Changes

Ada

Nichols²,

Levan³

1969

Annals of the New York Academy of Sciences

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Section: Single Breakssupporting

confidence: 85%

Virus‐induced Chromosome Changes

Ada

Nichols²,

Levan³

1969

Annals of the New York Academy of Sciences

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“…The mechanisms by which viruses induce chromosomal changes within infected host cells are still obscure. Both deoxyribonucleic acid (DNA) viruses (2, 8, 24) and ribonucleic acid (RNA) viruses (9,15,16) may cause such alterations. The replication site in the host cell, whether nuclear or cytoplasmic, also seems to be of no importance.…”

mentioning

confidence: 99%

Induction of Specific Chromosomal Aberrations by Adenovirus Type 12 in Human Embryonic Kidney Cells

Hausen

1967

J Virol

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Nonrandom chromosomal breaks in chromosomes 1 and 17 were provoked in human embryonic kidney cells 24 hr after infection with adenovirus type 12. These chromosomal changes disappeared in persistently infected cultures. Neutralization of the virus with type-specific antiviral serum prior to infection prevented the occurrence of chromosomal aberrations. No viral deoxyribonucleic acid (DNA) synthesis, as determined by autoradiography, was seen in metaphases containing adenovirus type 12-induced chromosomal aberrations. Ultraviolet irradiation of the virus reduced chromosomal aberrations linearly. This reduction in aberrations was fourfold slower than the inactivation of viral infectivity. At 24 hr after infection of cells with purified 3 H-labeled adenovirus type 12, the isotope was found to be associated with the nuclei. The uptake of isotope was reduced ninefold when the labeled virus was neutralized with type-specific antiviral serum. This difference is considered to account for neutralization of labeled virions. In metaphases infected with labeled viruses, most of the clustered grains were seen only on one arm of the chromatid, even after 72 hr. Isochromatid labeling was found, however, in a small percentage of chromosomes, and increased with time after infection. This increase was threefold between 24 and 72 hr after infection, whereas the mean grain counts decreased twofold during the same period. This has been tentatively interpreted to mean that most of the viral DNA molecules or parts thereof are merely attached to cellular chromatin, but a small fraction of them becomes gradually integrated as time proceeds. Certain chromosomal sites appeared to be preferentially labeled when chromosome 2 was used as a model for evaluation.

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“…Adult male volunteers vaccinated with the yellow-fever vaccine did not develop detectable antibodies to this contaminant virus. Some strains of Rous sarcoma virus, which is a member of this chicken tumour virus group, will infect human and simian tissues in vitro (Jensen, Girardi, Gilden & Koprowski 1964), produce chromosome abnormalities in human leukocytes (Nichols et al 1964) and even tumours in monkeys (Munro & Windle, 1963).…”

Section: Discussionmentioning

confidence: 99%