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At least 19 recordsLinked to original sources
PubMed1982

Mouse mammary tumour virus and polyoma virus information in mammary tumours of athymic mice inoculated with polyoma virus.

Polyoma virus inoculation of athymic mice results in the development of mammary tumours with a much higher incidence than the development of salivary gland tumours, the latter being the most common for immunocompetent normal mice. The possibility existed that polyoma virus might act as a co-carcinogen in activating the expression of mouse mammary tumour virus (MMTV). Molecular hybridization studies, however, showed that the mammary tumour development was accompanied by neither the amplification of MMTV genomic sequences nor by their more extensive transcription. In contrast, tumour tissue contained about 60 to 100 copies of polyoma virus genome equivalents per cell and some of these sequences were apparently transcribed into RNA. While these results do not rule out the transient involvement of MMTV expression in mammary tumour development, it appeared that the mammary gland cells were directly transformed by polyoma virus. Apparently, polyoma virus displayed a tropism in athymic mice that was different from that in normal mice.

Animals↗
PubMed1978

Further investigations on the antioncogenic activity of A/PR8/34 (HON1)- influenza virus on polyoma virus induced tumors in newborn Wistar rats.

The oncogenic activity of polyoma virus in newborn Wistar rats can be significantly reduced by simultaneous vaccination with the A/PR8/34 (HON1) strain of influenza virus. The antioncogenic activity (AOA) of influenza virus suspensions was neutralized by the addition of homologous influenza antibodies, indicating that AOA was due to influenza virus and not to any non-viral material possibly present. The AOA of influenza virus was found to decline with storage at 4 degrees C and to depend critically on the relative doses of influenza virus and polyoma virus inoculated per animal. Simultaneous inoculation of animals with influenza and polyoma virus reduced significantly the antibody response to polyoma virus in all experiments, suggesting that influenza virus reduced the multiplication of polyoma virus. By contrast, the antibody response to influenza virus was significantly enhanced by inoculation with polyoma virus in some experiments, only. Influenza virus was found to reduce markedly the adsorption of polyoma virus on rat embryo fibroblast cells, suggesting that AOA could be at least partially due to interference of influenza virus with polyoma virus adsorption on target cells.

Animals↗
PubMed1978

Detection of airborne polyoma virus.

Polyoma virus was recovered from the air of an animal laboratory housing mice infected with the virus. Air samples were obtained by means of a high volume air sampler and further concentrated by high speed centrifugation. Total concentration of the air samples was 7.5 x 10(7). Assay for polyoma virus was by mouse antibody production tests. Airborne polyoma virus was detected in four of six samples.

Air Microbiology↗
PubMed1983

The transforming gene of polyoma virus.

Polyoma virus appears to encode a transforming function. A variety of studies lead to the conclusion that this function resides mainly, and in some instances possibly exclusively, within the virally-coded middle T-antigen. Whereas this protein was originally isolated from membranes of cells infected with polyoma virus as a 55 kilodalton species, our recent studies, using monoclonal antibodies, suggest that middle T-antigen is a family of proteins, at least one member of which (but not all others) can be associated with a protein kinase activity. Investigation of the sub-cellular location of the middle T-antigen (s), using either immunofluorescence or immunoelectron-microscopy, and the monoclonal antibodies, show them to be associated with all cytoplasmic membranes. At early times post-infection, most of the middle T-antigen is found in association with the rough endoplasmic reticulum of the cell; only a few percent can be found located at the plasma membrane. At late times post-infection, this percentage increases. These data lead to the hypothesis that structurally similar viral proteins might have different functions, expressed at different locations within the cell. Which function(s) pertain to transformation remain to be defined.

Amino Acid Sequence↗
PubMed1980

Antioncogenic activity of influenza virus on polyoma virus induced renal and brain tumors in newborn Wistar rats.

Simultaneous inoculation of newborn Wistar rats with intact A/PR 8/34 (HON 1) influenza virus and the S.E. strain of polyoma virus resulted in significant reduction of the rates of both kidney sarcomas and brain tumors in comparison to controls given polyoma virus, only. This antioncogenic activity (AOA) of influenza virus was observed independently whether or not influenza and polyoma virus were injected on different sites or were inoculated as a combined vaccine. Ether-treated A/PR 8/34 influenza virus was found to have also AOA. However, in one experiment a significant AOA was demonstrated with respect to brain tumors, only, and not for the rate of renal sarcomas. In addition, the influenza strain A/Hong Kong/1/68 (H3N2) was found to have AOA.

Animals↗
PubMed1984

Detection of mutant-specific responses by macrophage migration inhibition reactions induced by wild-type and mutant polyoma viruses and polyoma virus-infected cells.

Macrophage migration inhibition responses of mice immunized with mutant polyoma viruses or with cells transformed and/or infected by them have been studied. The macrophage migration inhibition reaction revealed individual differences. In several cases, mice immunized with a mutant virus responded preferentially or exclusively to extracts of cells transformed or infected with the corresponding mutant. Moreover, in the macrophage migration inhibition test, mutant viruses were usually less immunogenic than were the corresponding transformed-infected cells.

Animals↗
PubMed1982

Improved infectivity of reassembled polyoma virus.

Polyoma virus was dissociated into capsomeres (18, 12, and 5S) and a DNA-protein complex (48S) with the Ca2+ chelator, ethyleneglycol-bis-N,N'-tetraacetic acid, and the reducing agent, 2-mercaptoethanol. The reaction was maintained at pH 5.0. Reassembly of the dissociated components to complete virions was accomplished by dialyzing these components overnight at 4 degrees C against the reassembly buffer containing CaCl2, dimethylsulfoxide, Triton X-100, and 0.01 M Tris-acetic acid (pH 5.0). Reconstructed particles ranged from 240S complete virions to lighter intermediate species. Approximately 25% of the dissociated particles could be physically reassembled to complete virions. These virions regained 12.5% of their hemagglutination ability and as much as 6.7% of their original infectivity. The infectivity of these reassembled particles represented a 100-fold increase in infectivity compared with that of the particles that were dissociated and reassembled at pH 7.4. Biochemical analysis showed that the polyoma viral receptor of the virions reassembled at pH 7.4 was greatly reduced, whereas virions reassembled at pH 5.0 retained their receptor. Reassembly could be further improved by additions of either exogenous capsomeres or DNA-protein complex to the reassembly reaction mixture.

Calcium Chloride↗
PubMed1976

Airborne transmission of polyoma virus.

Polyoma virus (PV) infection was transmitted through the air of an animal laboratory. Mice free of detectable antibodies to PV were exposed for 1 month to the airborne environment of laboratories housing naturally infected mice. The seroconversion rate was 75% (24/32), as measured by hemagglutination inhibition. Control mice, housed in the sterile atmosphere of a mass air flow cabinet (MAFC) in the same laboratory, had a seroconversion rate of 15.8% (3/19). Airborne transmission occurred bia PV aerosois, generated by the handling of contaminated bedding, cages, and mice during weekly housekeeping. Length of exposure to PV aerosols correlated with seroconversion. One- and 3-hour exposures resulted in seroconversion rates of 40% (6/15) and 72% (23/32), respectively. Seroconversion rates of mice continuously housed in MAFC totaled 5% (2/40). Checkerboarding mice free of detectable antibodies with mice given 10(5) mean tissue culture infective doses of PV ip resulted in an airborne infection rate of 50% (15/30) in a conventionally ventilated room during a 12-week study. The airborne transmission rate was 10% (3/30) when experiments were performed in a mass air flow room with a vertical air velocity of 30 feet/minute was used. Antibodies to PV could not be detected in any of 138 human sera, including sera from 29 animal-care technicians who handled PV-infected mice and 15 personnel who had worked with the virus.

Animals↗
PubMed1979

Lack of sequence homology between the nucleic acids of Rauscher leukaemia virus and polyoma virus Y8e produced simultaneously in a continuous mouse cell line.

In a continuous cell line (Y8e) from spleen and thymus cells of mice, infected with RLV, the presence of both RLV and polyoma virus Y8e in a single cell could be demonstrated by electron microscopy. A comparison of the nucleic acids of RLV and polyoma virus from Y8e cells by two molecular hybridization methods showed lack of sequence homology between the viral nucleic acids.

Animals↗
PubMed2001

Serological status for Chlamydophila psittaci, Newcastle disease virus, avian polyoma virus, and Pacheco disease virus in scarlet macaws (Ara macao) kept in captivity in Costa Rica.

From 1998 to 1999, a total of 128 blood samples were collected from scarlet macaws (Ara macao), kept in captivity in 11 different aviaries located in six provinces of Costa Rica. The sera were examined for antibodies directed against Chlamydophila psittaci, Newcastle disease virus (NDV), avian polyoma virus (APV), and Pacheco disease virus (PDV). Testing by enzyme-linked immunosorbent assay (ELISA), showed 16 (12.39%) of the samples (n = 129) exhibited antibodies directed against C. psittaci. Employing haemagglutination inhibition tests for NDV antibodies, all of the samples were found to be negative. The prevalence of antibodies specific for APV was tested with a blocking ELISA and serum neutralization tests (SNT) and 12 of 128 samples (9.37%) were found to be positive with both tests. In SNT, two out of 128 samples (1.56%) were positive for PDV. This is the first description of the serological status in scarlet macaws in captivity in Costa Rica. The study demonstrates the absence of NDV antibodies in the birds investigated on one hand, but also indicates a health hazard for numerous avian species due to the risk of infections with C. psittaci, APV or PDV.

Animals↗
PubMed2006

Renal transplant patient with polyoma virus bladder infection and subsequent polyoma virus nephropathy.

Polyoma virus nephropathy (PVN) is a significant cause of renal allograft dysfunction in transplant patients. A 58-year-old male received a cadaveric renal transplant and 12 weeks later presented with fever, diarrhea, and dysuria. He was diagnosed with a polyoma virus infection of the bladder by a transurethral bladder biopsy. One year post-transplant, he presented with renal allograft dysfunction and was diagnosed by biopsy with PVN of the non-native kidney. The diagnosis of a polyoma virus infection was confirmed by immunoreactivity to the polyoma T-antigen. We suggest that polyoma virus infection of the bladder be included in the differential diagnosis of urinary dysfunction in post-transplant patients, as such infections might be an under-recognized comorbidity in individuals with PVN.

Antigens, Polyomavirus Transforming↗
PubMed1969

Polynucleotide ligase activity in cells infected with simian virus 40, polyoma virus, or vaccinia virus.

The conversion of simian virus 40 (SV40) component II deoxyribonucleic acid to component I has been used to assay polynucleotide ligase in extracts of tissue culture cells. All cell types examined, including chicken, hamster, mouse, monkey, and human cells, contained adenosine triphosphate-dependent ligase. After infection of mouse embryo, monkey kidney, and HeLa cells with polyoma virus, SV40, and vaccinia virus, respectively, the enzyme activity increased, but its cofactor requirement was unchanged. In vaccinia virus-infected cells, the increased activity was localized in the cytoplasm. Ligase induction occurred in the presence of cytosine arabinoside but was prevented by puromycin. Rifampicin blocked the production of infectious vaccinia particles but had little effect on the induction of ligase.

Animals↗
PubMed1978

Infection of mouse preimplantation embryos with simian virus 40 and polyoma virus.

Mouse two-cell embryos, morulae, and blastocysts were killed when infected in vitro with simian virus 40 (SV40) at high multiplicities of infection. Polyoma virus was not deleterious for preimplantation embryos, even at a very high multiplicity of infection; however, the outgrowths of polyoma-infected blastocysts disintegrated after several days of culture. Indirect immunofluorescence tests revealed the presence of SV40 T and V antigens and polyoma virus V antigen in the nuclei of trophoblastic cells. Virus-specific antigens were not found in the nuclei of cells forming inner cell masses of blastocysts or in inner cell mass-derived cells in blastocyst out-growths. The appearance of SV40 T and V antigens in the nuclei was inhibited by alphaamanitin, a RNA polymerase II inhibitor. The amount of infectious virus recovered from cultures of morulae or blastocysts on subsequent days after infection with SV40 initially declined but later increased. These points of evidence indicate that some cells of early mouse embryos are permissive for the expression of early and late functions of SV40 genome and that susceptibility to infection with polyoma virus and/or permissiveness for the expression of polyoma virus late functions develop gradually between the two-cell and blastocyst stages. Electron microscope observations showed the presence of specific complexes of membranes and virions in the cytoplasm of trophoblastic cells. Single viral particles could be found in the nuclei and also in mitochondria.

Amanitins↗
PubMed1999

Cynomolgus polyoma virus infection: a new member of the polyoma virus family causes interstitial nephritis, ureteritis, and enteritis in immunosuppressed cynomolgus monkeys.

Polyoma virus infection causes acute interstitial nephritis and ureteral stenosis in humans but has rarely been noted in other species. In the present study, a hitherto unknown polyoma virus was detected in 12 of 57 cynomolgus monkeys after 3 to 11 weeks of immunosuppression given to promote acceptance of renal allografts or xenografts. This virus, termed cynomolgus polyoma virus (CPV), is antigenically and genomically related to simian virus 40 (SV40). The tubular epithelial nuclei of the collecting ducts in the medulla and cortex reacted with an antibody for the SV40 large T antigen and by electron microscopy contained densely packed paracrystalline arrays of 30- to 32-nm diameter viral particles. A polymerase chain reaction analysis of DNA extracted from affected kidneys detected polyoma virus sequences using primers for a highly conserved region of the large T antigen of polyoma virus. Sequence analysis showed 7 base substitutions and 3 to 5 deletions in the 129-nucleotide segment of amplified products, compared with the corresponding portion of SV40, yielding 84% homology at the amino acid level. CPV caused interstitial nephritis in six renal allografts, a xenograft kidney, and six native kidneys. Infected animals showed renal dysfunction and had tubulointerstitial nephritis with nuclear inclusions, apoptosis, and progressive destruction of collecting ducts. CPV was detected in the urothelium of graft ureters, associated with ureteritis and renal infection. Viral infection was demonstrable in smooth muscle cells of the ureteric wall, which showed apoptosis. One animal had diarrhea and polyoma virus infection in the smooth muscle cells of the muscularis propria of the intestine. Spontaneous resolution occurred in one case; no animal had virus detected in tissues more than 3 months after transplantation. Thus, immunosuppression predisposes cynomolgus monkeys to a polyoma virus infection with clinical consequences quite similar to BK virus infection in humans, including renal dysfunction. We also suggest that this may be the pathogenetic basis for the significant incidence of late onset, isolated ureteral stenosis observed in these recipients.

Animals↗
PubMed1975

Studies of polyoma virus DNA: cleavage map of the polyoma virus genome.

A small-plaque polyoma virus, MPC-1, was isolated from a mouse plasmacytoma. The DNA of this polyoma virus was cleaved with a restriction enzyme from Haemophilus influenzae (Hin d), and the molecular weights of the limit products were analyzed by electrophoresis and electron microscopy. The fragments produced by this enzyme have been ordered by analysis of partial digest products. A physical map of the polyoma virus genome was then constructed.

Animals↗
PubMed1980

Simian virus 40 and polyoma virus stimulate overall cellular RNA and protein synthesis.

In lytic infection with simian virus 40 and polyoma virus of monkey and mouse cells in tissue culture, synthesis of the viral tumor (T) antigens (T antigens) is rapidly followed by a mitogenic response of the host cell. The latter begins with virus-induced stimulation of overall cellular RNA and protein synthesis, leading to a substantial increase in cytoplasmic and nuclear RNA and protein. Stimulation begins within 1 hr after onset of T-antigen synthesis and also occurs if virus-induced DNA synthesis is blocked by metabolic inhibitors. The broad spectrum of biological and molecular effects induced by simian virus 40 and polyoma virus is, at least phenotypically, reminescent of the pleiotropic impact exerted on target cells by nonviral mitogens and by certain growth-promoting steroid and polypeptide hormones.

Antigens, Neoplasm↗