Immunofluorescent demonstration of a specific surface antigen in cells infected or transformed by polyoma virus

Irlin, I. S.

doi:10.1016/0042-6822(67)90051-7

Cited by 61 publications

(15 citation statements)

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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].…”

Section: Discussionsupporting

confidence: 76%

“…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]. In polyoma virus, too, the surface antigen(s) is synthesized as one of the early gene products, since it appears at a very early stage of infection prior to viral DNA synthesis [25,31].…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 76%

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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“…It has been possible to demonstrate antigenic modifications at the surface of these cells such as transplantation antigen (TSTA) (Habel, 1969), S antigen (Irlin, 1967;Meyer and Birg, 1970) revealed by immunofluorescence, and oncofoetal antigen.…”

mentioning

confidence: 99%

Biological activities of solubilized surface antigens of embryonic and polyoma-virus-transformed cells

Kitahara¹,

Barra²,

Meyer³

1978

Br J Cancer

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Summary.-Various antigenic activities of polyoma virus-transformed and embryonic mouse cells were retained after 3M KCl solubilization of surface components. Particularly, transplantation antigen (TSTA) demonstrated by homograft rejection, and surface (S) antigen, detected by inhibition of immunofluorescence on polyomavirus-transformed mouse cells, could be demonstrated. The crude soluble extracts were partially purified by salting out with (NH4)2SO4. In the case of polyoma-virustransformed cells, TSTA and a part of S antigen activity were found in the same fraction (60% (NH4)2SO4 saturation) while another part of S antigen was salted out at 80% saturation. By chromatography, S antigen activity was found in 2 zones for transformed cells and in one zone for embryonic cells. One of these zones was common to both cell extracts.

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“…Deoxyribonucleic acid (DNA) virus-specific surface or membrane antigens induced on established cell cultures or on tumor cells by oncogenic viruses such as simian virus 40, polyoma, EpsteinBarr, Shope papilloma, and herpesvirus of Marek's disease (2,4,8,9,11,12,17), and by nononcogenic agents, i.e., some poxviruses of the vaccinia group (15,18), have been demonstrated by the immunofluorescence technique. Other than the detection of a new cell surface antigen in Moloney virus-induced lymphomas and in cell cultures (10,16), reports of similar findings with other ribonucleic acid (RNA) oncogenic or nonocogenic viruses are limited (19).…”

mentioning

confidence: 99%

“…Formation of the antigen was independent of viral ribonucleic acid synthesis.Deoxyribonucleic acid (DNA) (2,4,8,9,11,12,17) (Fig. 1); uninfected cells did not fluoresce.…”

mentioning

confidence: 99%

Cell-Surface Antigen Induced by Venezuelan Equine Encephalomyelitis Virus

Hahon¹

1970

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By immunofluorescence staining, a specific surface antigen induced by Venezuelan equine encephalomyelitis virus was detected on L-929 cells. Formation of the antigen was independent of viral ribonucleic acid synthesis.Deoxyribonucleic acid (DNA) (2,4,8,9,11,12,17) (Fig. 1); uninfected cells did not fluoresce. The specificity of the staining was confirmed by the absence of surface fluorescence on cells infected with VEE virus and stained with variola, chikungunya, or yellow fever fluorescein-conjugated antiviral serum. Similar results were obtained when cell monolayers were infected with any of these three viruses and stained with conjugated VEE antiserum. Further incidence of staining specificity was obtained by demonstrating that cell surface antigen fluorescence was blocked when cells were first treated with unlabeled monkey antiviral serum prior to staining with conjugated antiviral serum. Induction of cell-surface antigen was not limited as to the source of virus, the strain of virus, or the L-929 cell line; the phenomenon was elicited by both infective mouse brain and chick embryo preparations, by two different attenuated VEE virus strains (1, 7), and on guinea pig lung, McCoy, and baby hamster kidney (BHK21 /C13) cell lines. Induction of cell surface antigen by VEE virus is dependent on the presence of infectious virus particles. Virus inactivated by either ultraviolet irradiation or heat (56 C, 16 hr) failed to induce the formation of cell surface antigen. Furthermore, the number of cells showing surface antigen was reduced approximately 93% when virus was mixed with antiviral serum before it was added to cell monolayers. Additional evidence that the manifestation of cell surface antigen is associated with the presence of infectious virus particles was noted by the demonstration of a linear relationship between relative virus concentration and the number of cells showing surface antigen. This finding suggests that each cell exhibiting fluorescent surface antigen results from infection by a single infective virion or aggregate not divisible by dilution. The dependency of surface antigen induction on viable virus is consistent with observations on the direct association between infection or production (or both) of Epstein-Barr virus and cell membrane antigen (4).To compare the rate of appearance of fluores-713

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Immunofluorescent demonstration of a specific surface antigen in cells infected or transformed by polyoma virus

Cited by 61 publications

References 6 publications

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

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

Biological activities of solubilized surface antigens of embryonic and polyoma-virus-transformed cells

Cell-Surface Antigen Induced by Venezuelan Equine Encephalomyelitis Virus

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