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The Immunological System and Neoplasia
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Several DNA viruses can transform cells in vitro or after inoculation of experimental animals. For example, polyoma virus, belonging to the family Papovaviridae, is capable of transforming cells in vitro as well as inducing tumors after inoculation of newborn mice and hamsters. One of the polyoma viruses, simian virus (SV)40, attracted the attention of tumor virologists when it was learned that a large number of humans were vaccinated with polio vaccine prepared in cell cultures contaminated with SV40. Fortunately, there is no evidence that SV40 causes cancer in humans. The mechanism of transformation by SV40 has been well studied. Cells can only be transformed by SV40 if the cells are nonpermissive for virus replication but allow early gene products to be made. One of these gene products called “middle T antigen” acts as a receptor for a growth factor, which causes constitutive activation of the cell cycle. The importance of polyoma viruses for tumor immunology was the finding that these tumors express virally induced tumor-specific antigens—a fact which was used in early studies on tumor rejection. Based on our current knowledge of the transformation process by polyoma viruses, it is clear that these immune responses are probably directed toward the “T antigen” family.
Viral neuro-oncogenesis: Polyomaviruses and brain tumors
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Martyn K. White, Sidney E. Croul, Kamel Khalili
Although still a controversial hypothesis, the initial evidence that human brain tumors might be associated with polyomavirus infection came from retrospective analyses of tumor incidence vs. SV40 polio vaccine contamination [20–23]. The rationale for these studies was the isolation of the SV40 virus in 1960. This was followed fairly rapidly by the recognition of SV40 contamination of previous oral polio vaccines and the oncogenic potential of SV40 in experimental systems. From its initial manufacture in 1954 until 1960, the Salk polio vaccine was grown on monolayers of rhesus monkey kidney cells, which were then treated with graded concentrations of formalin to inactivate virus infectivity but preserve antigenicity. Because SV40 is found frequently in rhesus monkeys but is more resistant to formalin inactivation than polio, it is not surprising that high titers of live virus were found in several batches of the vaccine. The administration of SV-40-contaminated polio vaccine was eliminated by 1961. It is not known how many of the 90 million people who were given the Salk vaccine were exposed to SV40, but estimates between 10 million and 30 million have been made [25].
Eukaryotic Dna-Dependent Rna Polymerases: An Evaluation of Their Role in the Regulation of Gene Expression
Published in Gerald M. Kolodny, Eukaryotic Gene Regulation, 2018
Trevor J. C. Beebee, Peter H. W. Butterworth
It is generally accepted that form II transcribes HnRNA (the putative precursor of mRNA) in its nucleoplasmic locus, and extensive studies both in vivo and in vitro using α-amanitin support this view.28 Much of this evidence is circumstantial, but direct confirmation has emerged from a number of different approaches to the problem. Mutants have been produced in Chinese hamster ovary cells53 and a BHK cell line54 which contain an α-amanitin-insensitive form II RNA polymerase. Whereas the expression of polyoma virus genes in infected mouse 3T3 cells is inhibited by α-amanitin in the growth medium, somatic cell hybrids between these infected cells and the α-amanitin-resistant BHK cell mutant results in the α-amanitin-insensitive expression of polyoma functions.54 This implies the direct involvement of form II polymerase in the transcription of viral messenger RNAs. Furthermore, SV40 can be isolated from infected mammalian cells in a form which contains polymerase II as a transcription complex.55 An alternative approach has been to raise antibodies to form II polymerase of Drosophila melanogaster56 and to show that these antibodies bind in the chromosomal interband regions and puffs which are known to be transcriptionally active in the larval salivary gland, adding further weight to the conclusion that form II is involved in mRNA synthesis.
BK virus in kidney transplant recipients with graft dysfunction
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Doaa Mohamed Riad, Wafaa Kamel Mowafy, Hazem Hamed Saleh, Essam Mahmoud El Sawy, Noha Tharwat Abou El-Khier
Urine cytology: Cytology smears from urine samples of case group were performed. Standard smears were prepared from fresh voided morning urine samples, fixed in alcohol, and stained with Papanicolaou stain. When positive for Decoy cells, the number of cells was counted (Figure 1).Renal graft biopsies: Renal graft biopsies were performed for all patients in the case group.Immunostaining with SV40 m-Ab: SV40 m-Ab from Santa Cruz Biotechnology (USA) was used.
Mesothelioma mortality within two radiation monitored occupational cohorts
Published in International Journal of Radiation Biology, 2022
Michael T. Mumma, Jennifer L. Sirko, John D. Boice, William J. Blot
Suspected non-asbestos risk factors for malignant mesothelioma include ionizing radiation (high-dose radiotherapy and Thorotrast (i.e. radioactive thorium dioxide that emits alpha particles)), viral infections (e.g. SV40), genetic predisposition (e.g. germline mutations of the BRCA1-associated protein 1), chronic pleural inflammation, and erionite (a naturally occurring fibrous material similar to asbestos). These factors may act alone or as co-factors together with asbestos or with ‘naturally occurring asbestos-like material’ such as erionite, to cause mesothelioma (Crew et al. 2005; Carbone et al. 2012, 2016; Attanoos et al. 2018). Animal experiments have shown the co-carcinogenic properties of high-dose radiation with asbestos (Warren et al. 1981). The polyomavirus simian virus 40 (SV40) has been reported to induce mesothelioma and to be a co-factor for asbestos carcinogenesis in experimental animals; however, the evidence for a causal relationship between SV40 and mesothelioma in humans is lacking (Carbone et al. 2012). Chronic inflammation appears to promote the occurrence of asbestos-related mesothelioma (Carbone and Yang 2017). Mesothelioma may thus be a multifactorial disease and not all non-asbestos causes may have been identified nor have all co-factor mechanisms.
Management of BK-virus infection – Swedish recommendations
Published in Infectious Diseases, 2019
Tina Dalianis, Britt-Marie Eriksson, Marie Felldin, Vanda Friman, Anna-Lena Hammarin, Maria Herthelius, Per Ljungman, Johan Mölne, Lars Wennberg, Lisa Swartling
A renal biopsy is mandatory to verify the diagnosis of BKVAN and should be performed upon increasing serum-creatinine levels and/or the finding of >10,000 BKV DNA copies/mL in serum/plasma. The morphological findings of BKVAN in the kidney vary depending on when after transplantation the infection is diagnosed. The diagnosis is based on immunohistochemistry using antibodies directed against SV40 (which in turn cross-react with BKV) (Figure 1). BKVAN is graded into classes 1–3, depending on the grade of fibrosis and the numbers of infected cells [10]. In biopsies, it may be difficult to distinguish between BKVAN in the absence vs. the presence of acute rejection. The morphology may actually be quite similar. The presence of inflammation in arteries (endarteritis) and/or microvascular inflammation suggests the presence of an acute rejection together with BKVAN.