Localization of SV40 T antigen in mitotic cells by an immunoperoxidase method

The immunoperoxidase technique has clearly demonstrated that SV 40 T antigen is dissociated from the chromosomes in mitotic cells, and massive transport of T antigen from the cytoplasm to the nucleus appears to take place during or immediately after the telophase.     

Localization of SV40 T antigen in mitotic cells by an immunoperoxidase method

Summary The immunoperoxidase technique has clearly demonstrated that SV40 T antigen is dissociated from the chromosomes in mitotic cells, and massive transport of T antigen from the cytoplasm to the nucleus appears to take place during or immediately after the telophase.     

Influences of cell cycle on uptake of SV40-DNA by diploid human cells

Zusammenfassung Autoradiographische Untersuchungen an menschlichen, diploiden, synchronisierten Zellen, in der S-Phase mit Tritium markiertem SV40 infiziert, zeigten intranukleären Einbau von markierter DNS (in Metaphase vor allem Chromosomenmarkierung). Keinerlei Kernmarkierung wurde beobachtet, wenn die Zellen in anderen Phasen ihres Zyklus infiziert wurden.

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This work was supported, in part, by a grant from the James W. McLaughlin Fund. Our thanks are due to Dr.K. G. Weiss for the valuable help in preparing the German summary.     

SV40 association with human malignancies and mechanisms of tumor immunity by large tumor antigen

SV40 was discovered as a contaminate of poliovirus vaccine lots distributed to millions of individuals in the United States between 1955 and 1963 while contaminated vaccine batches were later circulated worldwide. After SV40 was observed to cause in vitro animal and human cell transformations and in vivo tumor formations in animals, the search for a connection between the virus and human malignancies has continued to the present day. Different molecular methods have been used to detect SV40 gene products in a variety of human cancers, though SV40 causality in these tumor types has yet to be established. These data, however, are not without controversial issues related to inconclusive SV40 serological and epidemiological evidence alongside tools and methodologies that may contribute to false-positive results in human specimens. This review will also explore how vaccination against SV40 protein products may be used to help prevent and treat individuals with SV40-expressing cancers. Received 19 September 2006; received after revision 8 November 2006; accepted 13 December 2006     

Simian virus 40 infection of uninoculated african green monkeys (Cercopithecus aethiops) revealed by repeated cell passages

Résumé Nous avons trouvé le virus SV₄₀ chez le singeCercopithecus aethiops présumé non infecté. Par la méthode de culture des cellules du rein et en effectuant des passages rapides nous avons pu démontrer l'existence du virus même chez les animaux dépourvus d'anticorps et même dans le cas où le virus n'apparaissait pas durant le premier passage.     

Induction, by 5-bromo-2'-deoxyuridine, of a "foamy" virus previously undetected in hamster cells transformed by SV40]

TSV5 clone 2 cells in normal conditions of culture contain only an expressed RNA virus (R-type virus). However, exposure of the cells to 5-bromo-2'-deoxyuridine with dexamethasone, induced synthesis of a syncitium-forming ("Foamy") virus. In other hamster cell lines, the same treatment fails to induce a "foamy" virus. The origin of this "foamy" virus is discussed.     

Serum activity inhibiting specific simian virus 40-induced transplantation resistance and its correlation with primary SV40 tumors appearance in hamsters

Summary Using the modified technique of transplantation test, ITR serum activity was found in most (14 out of 21) individual hamster sera obtained during the latent period of primary SV40 carcinogenesis (60 days after virus infection when newborn). On the other hand, as a rule, no ITR activity was observed in the sera of the same hamsters after tumor appearance and during their growth. ITR activity rapidly disappeared from sera of hamsters neonatally infected with SV40 after their successful immunization with the same virus during the latent period. There appears to be a correlation between the presence of ITR serum factor during the latent period and the subsequent primary SV40 tumor appearance in hamsters.Acknowledgment. The author wishes to thank Dr Galina I. Deichman for continuing advice and encouragement during the course of these studies.     

Serum activity inhibiting specific simian virus 40-induced transplantation resistance and its correlation with primary SV40 tumors appearance in hamsters.

Using the modified technique of transplantation test, ITR serum activity was found in most (14 out of 21) individual hamster sera obtained during the latent period of primary SV40 carcinogenesis (60 days after virus infection when newborn). On the other hand, as a rule, no ITR activity was observed in the sera of the same hamsters after tumor appearance and during their growth. ITR activity rapidly disappeared from sera of hamsters neonatally infected with SV40 after their successful immunization with the same virus during the latent period. There appears to be a correlation between the presence of ITR serum factor during the latent period and the subsequent primary SV40 tumor appearance in hamsters.     

OX40 promotes obesity-induced adipose inflammation and insulin resistance

Adaptive immunity plays a critical role in IR and T2DM development; however, the biological mechanisms linking T cell costimulation and glucose metabolism have not been fully elucidated. In this study, we demonstrated that the costimulatory molecule OX40 controls T cell activation and IR development. Inflammatory cell accumulation and enhanced proinflammatory gene expression, as well as high OX40 expression levels on CD4⁺ T cells, were observed in the adipose tissues of mice with diet-induced obesity. OX40-KO mice exhibited significantly less weight gain and lower fasting glucose levels than those of WT mice, without obvious adipose tissue inflammation. The effects of OX40 on IR are mechanistically linked to the promotion of T cell activation, Th1 cell differentiation and proliferation—as well as the attenuation of Treg suppressive activity and the enhancement of proinflammatory cytokine production—in adipose tissues. Furthermore, OX40 expression on T cells was positively associated with obesity in humans, suggesting that our findings are clinically relevant. In summary, our study revealed that OX40 in CD4⁺ T cells is crucial for adipose tissue inflammation and IR development. Therefore, the OX40 signaling pathway may be a new target for preventing or treating obesity-related IR and T2DM.     

Stimulation of SV40 virus replication in Chinese hamster kidney cells by treatment of the cells with mitomycin C]

The production of virions by Chinese hamster kidney cells infected with SV 40 DNA is increased 10 to 100 fold by mitomycin C treatment. This observation has been confirmed for different cell clones. The optimum concentration of mitomycin C has been determined.     

Regulation of cell adhesion by PP2A and SV40 small tumor antigen: An important link to cell transformation

The serine/threonine protein phosphatase 2A (PP2A) represents a large family of highly conserved heterotrimeric enzymes. Their critical importance in cell homeostasis is underlined by the fact that they are targets of natural toxins like the tumor promoter okadaic acid, and of simian virus 40 small tumor antigen (SV40 small t), a viral protein known to promote cell transformation. Furthermore, mutated or lower expression levels of PP2A subunits have been found in certain cancers. One major known event in PP2A-dependent cell transformation is the alteration of key signaling pathways that control cell growth and survival. In this review, we focus on how PP2A enzymes also affect cell adhesion and cytoskeletal dynamics, the disruption of which is linked to loss of cell polarity, increased cell motility and invasiveness. We also examine how those various pathways participate in the transforming activity of SV40 small t. Received 29 June 2006; received after revision 3 August 2006; accepted 20 September 2006