Activation of production of infectious tumor virus SV40 in heterokaryon cultures (original) (raw)
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Rescue of infectious SV40 after fusion between dfferent SV 40-transformed cells
Proceedings of the National Academy of Sciences, 1968
We have previously reported' activation of infectious SV40 in transformed cell types of various origins after fusion with susceptible African green monkey kidney cells (AGMK). In the same report, we described failure to activate SV40 after fusion of AGMK cells with two sublines of SV40-transformed human cells (W98-VaC and WI26Va4) and cultures originating from four clones of SV40-transformed green monkey kidney cells (GMK-EVa).
Genes & cancer, 2010
SV40 has been detected prevalently in a limited panel of human tumors: mesothelioma, bone and brain tumors, and lymphoma. These are the same tumor types that are specifically induced by SV40 when injected into hamsters, a finding that has raised concerns about the possible pathogenic role of SV40 in humans. Two different SV40 isolates differing in the number of 72-bp elements in the virus regulatory region, archetypal SV40 (1ESV40), which contains one 72 bp, and nonarchetypal SV40 (wtSV40), which contains two 72 bp, have been detected in human tumors. 1ESV40 has been prevalently detected in brain tumors, with wtSV40 prevalently in mesothelioma. The apparent different cell tropism could be related to the virus (i.e., possibly to the number of 72-bp elements) and to different expression of cellular genes, known to play a critical role in SV40-mediated transformation of human cells, such as Notch-1 and c-Met. To test for possible differences in tissue tropism, we infected primary human...
Cell, 1984
A murine retroviral vector has been used to separate physically the overlapping genes encoded by SV40. This minimal retroviral vector contains LTRs and other c&acting signals required for infectious RNA virus propagation. We placed the SV40 early region within this DNA and after transfection of cells producing helper Moloney murine leukemia virus, SV40 retroviruses (MV40) could be rescued. Cytoplasmic spliced large T and small t transcripts, as well as unspliced transcripts, are packaged into virions with equal efficiency. Pure SV40 large T retroviruses can be cloned from these heterogeneous virus stocks by secondary transformation of rodent cells. The large T retrovirus stocks morphologically transform primary or established mouse and rat lines with high efficiency. There is little difference in transformation either by agar assay or focus formation between retroviruses carrying both SV40 genes or large T alone. We present quantitative data that demonstrate that abortive transformation of rodent cells by SV40, transient expression of the transformed phenotype after infection, is not manifested by MV40. Thus abortive transformation is not the result of a weakly dominant transforming gene, but rather of the normally inefficient mode of integration and early gene expression of SV40 upon infection of rodent cells.
The role of the SV40 ST antigen in cell growth promotion and transformation
Seminars in Cancer Biology, 2001
The simian virus 40 small-t (ST) antigen plays a key role in permissive and nonpermissive infections, increasing virus yields in lytic cycles of primate cells and enhancing the ability of large-T (LT) to transform rodent or even human cells. In the absence of ST, tumors in rodent model systems appear primarily in lymphoid and other proliferative tissues and transformation is
Proceedings of the National Academy of Sciences, 1968
During the investigation of the action of SV40 virus by means of fusion of SV40-transformed cells with virus-susceptible monkey kidney cells,' it became apparent that SV40-induced complement fixation antigen (ICFA)2 was transmitted to the nuclei of the nontransformed cells whether or not fusion between the two systems resulted in the isolation of infectious virus.' 3 This was not surprising, since the mechanism of ICFA synthesis apparently is unrelated to the synthesis of viral protein and infectious virus, and the antigen is found in many non-virus-yielding transformed cells. As a corollary of these observations, an investigation of transmission of ICFA in heterokaryocytes to nuclei originating from cells resistant to SV40 infection became of interest. Further, a study of the mechanism of the transmission of ICFA was instituted to elucidate the process of its intracellular synthesis.
Variable expression of SV40 large T antigen in CV1 cell clones
FEBS Letters, 1988
Using immunofluorescence and immunoadsorption, CVl cell clones MA2, V4, USA3, TR7 and P3 infected with SV40 were found to express variably SV40 large T antigen. The monoclonal antibody used was Pab 419. The results indicate that P3 cells express T antigen to a considerable level as early as 10 h post-infection, while that of TR7 and USA3 cells is minute as judged from their positive nuclei. MA2 and V4 cells did not show any positive nuclei over this period of infection. At 20 h post-infection MA2, V4 and USA3 cells developed a considerable amount of fluorescence in their nuclei while TR7 and P3 cells produced high values. By immunoadsorption of cell extracts for the same periods of infection, similar results were obtained on the electrophoretograms. We also relate these findings with those from induction of heatshock proteins by SV40 infection.