Inactivation, by UV-, X-, and γ-radiations, of the infecting and transforming capacities of polyoma virus

Latarjet, R; Cramer, Robert A.; Montagnier, Luc

doi:10.1016/0042-6822(67)90098-0

Cited by 83 publications

(31 citation statements)

References 19 publications

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“…Latarjet, Cramer & Montagnier (1967) showed that infectivity of polyoma virus and its transformation capacity are equally resistant to the direct effect of ioniy.ing radiations. The different results obtained by Benjamin (1965) and by Basilico & Di Mayorca (1965) would be due to the indirect effect not being entirely suppressed.…”

Section: Discussionmentioning

confidence: 99%

Infectivity and Capacity for DNA Replication of Vaccinia Virus Irradiated by -Rays

Decker¹,

Guir²,

Kirn³

1969

Journal of General Virology

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SUMMARYPurified vaccinia virus was irradiated by 7-rays under direct-effect conditions. The ability of the irradiated samples to form plaques (infectivity) and to induce viral DNA synthesis was determined. The radiosensitive volume of the viral unit causing infection (I.9 × IO-X7 cm2) is very small compared with the volume of the whole viral DNA (~ IO %).The inactivation of the D N A replication function follows a simple exponential law. The radiosensitive volume necessary for the replication of DNA (1-6 × IO -is cm. a) represents only 8"5 % of the DNA necessary for infectivity and o'85 % of the total viral DNA. This indicates existence of a dissociation between two functions of vaccinia virus, the synthesis of viral DNA and infectivity.

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Section: Discussionmentioning

confidence: 99%

Infectivity and Capacity for DNA Replication of Vaccinia Virus Irradiated by -Rays

Decker¹,

Guir²,

Kirn³

1969

Journal of General Virology

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“…The appearance of a surface antigen or antigens in virus-infected cells was independently reported in polyoma virus [25,31] and in SV40 [15,28] at about the same time as our reports or a few years later. In both viruses only 1/5-1/2 or the whole viral genome was estimated to be necessary for cell transformation by determining sensitivity to X-ray, y-ray and ultraviolet irradiations and to inactivation by nitrous acid and by 32P decay [4][5][6]29]. The proportions of early and late genes have been estimated to be about 35% and 65% of the whole SV40 genome, respectively, and about 60% of the early genes and about 10% of the late genes have been estimated to be transcribed in SV40-transformed or tumor cells which carry TSTA and S antigens [27][28][29].…”

Section: Discussionmentioning

confidence: 99%

“…In both viruses only 1/5-1/2 or the whole viral genome was estimated to be necessary for cell transformation by determining sensitivity to X-ray, y-ray and ultraviolet irradiations and to inactivation by nitrous acid and by 32P decay [4][5][6]29]. The proportions of early and late genes have been estimated to be about 35% and 65% of the whole SV40 genome, respectively, and about 60% of the early genes and about 10% of the late genes have been estimated to be transcribed in SV40-transformed or tumor cells which carry TSTA and S antigens [27][28][29]. This part of viral DNA transcribed in SV40 tumor cells approximates the part of viral DNA transcribed in adenovirus tumor cells [9-13, 17], and in both cases, early genes are mainly transcribed [34][35][36]38].…”

Section: Discussionmentioning

confidence: 99%

Tumor‐Specific Transplantation Antigen Activity of Freshly Adenovirus‐Infected Cells

Nakajima

Hamada

Uetake

1974

Japanese Journal of Microbiology

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Newborn hamsters were inoculated with human adenovirus type 12 (Ad 12) within 24 hr of birth for tumor induction, and 15 days later, intercurrently immunized with Ad12-infected cells (KB; HeLa; FL; HEK; MoE; HaE).Tumor development was then observed for 75 days thereafter. Tumor formation was prevented at a statistically significant level by immunization with any of the above-mentioned infected cells. The immunization was effective even with abortively infected cells (HaE; MoE) or with cells infected in the presence of 5-fluorodeoxyuridine. The induced immunity was Ad 12-specific, since neither cells infected with Ad2, Ad7 or Ad18 nor CV-1 cells infected with SV40 were able to prevent tumor formation. The most plausible explanation to these findings could be that Ad 12-specific tumor-specific transplantation antigen is induced on the surface of freshly virus-infected cells and it is responsible for induction of specific cellular immunity. This gives an experimental support to our hypothesis on the mechanism of induction of cellular immunity against virus infections and to the hypothesis proposed by Habel and by Sjogren to explain the immunoresistance against tumor cells induced following viral immunization.

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“…In most viruses the other major constituents of the virus particles play relatively minor roles in inactivation by UV (55). For example, whole MS2, f2, Q␤, encephalomyocarditis virus (EMCV), and murine polyoma viruses and their respective free nucleic acids have essentially the same UV 254 sensitivities (14,30,75,80,86). (Virus abbreviations are those indicated in the Virus Taxonomy report [76].)…”

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confidence: 99%

Predicted Inactivation of Viruses of Relevance to Biodefense by Solar Radiation

Lytle

Sagripanti

2005

J Virol

279

358

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UV radiation from the sun is the primary germicide in the environment. The goal of this study was to estimate inactivation of viruses by solar exposure. We reviewed published reports on 254-nm UV inactivation and tabulated the sensitivities of a wide variety of viruses, including those with double-stranded DNA, single-stranded DNA, double-stranded RNA, or single-stranded RNA genomes. We calculated D 37 values (fluence producing on average one lethal hit per virion and reducing viable virus to 37%) from all available data. We defined "size-normalized sensitivity" (SnS) by multiplying UV 254 sensitivities (D 37 values) by the genome size, and SnS values were relatively constant for viruses with similar genetic composition. In addition, SnS values were similar for complete virions and their defective particles, even when the corresponding D 37 values were significantly different. We used SnS to estimate the UV 254 sensitivities of viruses for which the genome composition and size were known but no UV inactivation data were available, including smallpox virus, Ebola, Marburg, Crimean-Congo, Junin, and other hemorrhagic viruses, and Venezuelan equine encephalitis and other encephalitis viruses. We compiled available data on virus inactivation as a function of wavelength and calculated a composite action spectrum that allowed extrapolation from the 254-nm data to solar UV. We combined our estimates of virus sensitivity with solar measurements at different geographical locations to predict virus inactivation. Our predictions agreed with the available experimental data. This work should be a useful step to understanding and eventually predicting the survival of viruses after their release in the environment.

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Inactivation, by UV-, X-, and γ-radiations, of the infecting and transforming capacities of polyoma virus

Cited by 83 publications

References 19 publications

Infectivity and Capacity for DNA Replication of Vaccinia Virus Irradiated by -Rays

Infectivity and Capacity for DNA Replication of Vaccinia Virus Irradiated by -Rays

Tumor‐Specific Transplantation Antigen Activity of Freshly Adenovirus‐Infected Cells

Predicted Inactivation of Viruses of Relevance to Biodefense by Solar Radiation

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