SV40 reporter viruses

Abstract

Three simian virus 40 (SV40) reporter viruses were constructed in this study. One expresses the green fluorescent protein (GFP) as a fusion protein with the first exon of large-T (LT) antigen and is useful for live-cell imaging. A second reporter virus has a FLAG epitope tag at the C-terminus of large-T (LT) antigen (vC-LT FLAG ), and a third has the FLAG tag at the N-terminus of LT (vN-LT FLAG ). The vC-LT FLAG construct grows to titers near those of wild-type (WT) virus and functions well as a reporter virus for SV40 infection. The vN-LT FLAG construct, while viable, has a defect in the production and spread of infectious particles. All three viruses are useful in detecting superinfecting virus in cells in which nuclear LT is already present, such as persistently infected human mesothelial cells.

Association Between Simian Virus 40 and Human Tumors

“…Mammalian cells of different histotypes behave toward SV40 infection in different ways, depending on the ability of this oncogenic polyomavirus (PyV) to complete the viral cycle and produce a mature viral progeny. SV40-infected cells can be (i) permissive, (ii) non-permissive, or (iii) semi-permissive (56, 58–60). The main discriminant depends on viral DNA replication potential expressed in permissive and semi-permissive cells.…”

“…In this case, viral progeny is produced, whereas SV40 infected cells lyse and die. CV-1 and fibroblast-like COS cell lines, both derived from monkey kidney tissue, are the prototype of permissive cells (58, 61). In non-permissive cells, no productive viral cycle is established, whereas the infection occurs but is abortive.…”

“…However, this PyV has not been reported in tumors of the rhesus macaque (Macaca mulatta), which is its natural host. Indeed, SV40 infection in permissive monkey cells derived from kidney tissues leads to cell lysis and death, without neoplastic transformation (58, 61). By contrast, SV40 experimentally inoculated in hamsters induces tumors of different histotypes, depending of the route of injection.…”

“…These results suggest that a few cells, found to be SV40-positive, induce SV40-negative cells on the microenvironment toward the transformation. The SV40-infected cells have also been determined by several in vitro studies (56, 58–65). Different hypotheses have been formulated on the mechanisms of SV40 carcinogenesis in human, including the “hit and run mechanism” which has been investigated in transgenic mice (274).…”

How Epstein-Barr Virus Induces the Reorganization of Cellular Chromatin

“…In order to understand ROCC further, we have explored it comparatively. We examined EBV’s ROCC in cells cotransfected with simian virus 40 (SV40), a DNA virus that packages chromatinized DNA and does not support ROCC ( 22 , 23 ). We found that cells in which the first step of ROCC has been triggered do not support SV40 DNA amplification.…”