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Infection and Immunity Jun 1972A new member of the papovavirus group has been isolated and appears to infect swine. The new agent, tentatively named swine papovavirus, appears to be very defective and...
A new member of the papovavirus group has been isolated and appears to infect swine. The new agent, tentatively named swine papovavirus, appears to be very defective and replicates only within a very narrow host cell range. The original source of the isolate is under investigation. Preliminary evidence suggests that the origin of swine papovavirus is either a stable pig kidney cell line or pancreas-derived trypsin
Topics: Animals; Antibodies, Viral; Cell Line; Centrifugation, Density Gradient; DNA, Viral; Dogs; Ethers; Fluorescent Antibody Technique; Humans; Kidney; Mice; Microscopy, Electron; Neutralization Tests; Nucleic Acids; Papillomaviridae; Polyomaviridae; Polyomavirus; RNA, Viral; Swine; Swine Diseases; Temperature; Vibration
PubMed: 4344097
DOI: 10.1128/iai.5.6.961-967.1972 -
Journal of Virology Jul 1968The simian papovavirus SV40 replicated as well in simian cells incubated at 41 C as in cells incubated at 37 C, although the latent period was shortened at the elevated...
The simian papovavirus SV40 replicated as well in simian cells incubated at 41 C as in cells incubated at 37 C, although the latent period was shortened at the elevated temperature. Human adenoviruses differed in their responses to the elevated temperature. Some serotypes, such as 3, 4, 5, 7, 8, 16, and 21, replicated as well, or almost as efficiently, in human cells incubated at 41 C as in cells incubated at 37 C, whereas with other serotypes, such as 1, 2, 6, 12, and 14, maximal yields in cultures incubated at 41 C were much lower than the yields from companion cultures incubated at 37 C. This difference was also detected in simian cells co-infected with SV40 and a human adenovirus; maximal complementation occurred with some serotypes at the elevated temperature but not with other serotypes. The degree of complementation observed in the simian cells at 41 C was directly correlated with the ability of the adenovirus to replicate at 41 C in human cells. Therefore, the capacity of SV40 to serve as a helper virus is not affected by the elevated temperature, showing that the complementation event supplied by the simian virus is heat-stable between 37 and 41 C. Maximal complementation appeared to depend upon a characteristic present in the adenovirus genome.
Topics: Adenoviridae; Animals; Culture Techniques; Embryo, Mammalian; Haplorhini; Humans; Kidney; Methods; Simian virus 40; Temperature; Virus Replication
PubMed: 4301993
DOI: 10.1128/JVI.2.7.670-677.1968 -
Journal of Virology May 1989Transgenic mice have been generated which carry the early region of lymphotropic papovavirus (LPV). Eight of eleven founder animals died before 3 months of age after...
Transgenic mice have been generated which carry the early region of lymphotropic papovavirus (LPV). Eight of eleven founder animals died before 3 months of age after developing one or both of two distinct proliferative disorders. Of the three surviving animals, two are known to have rearranged or partial copies of the LPV genes. The majority of the founder animals (six) developed debilitating choroid plexus tumors by 26 to 42 days. Although this is the same tumor type induced by the simian virus 40 T-antigen gene, those induced by LPV appeared at a much younger age. The LPV early region was expressed in the brain tumors of these mice, as well as in the thymus and spleen. Expression in the latter two tissues reflects the cell-type specificity of the LPV enhancer demonstrated in cultured cells (i.e., lymphoid cells). Two founder animals (LP41 and LP50) gave rise to lines of mice that routinely develop lymphoproliferative disorders. LP50 and its LPV-positive offspring developed aggressive lymphomas and choroid plexus tumors. The transgenic offspring of LP41 also developed lymphomas. High levels of LPV RNA were expressed in the lymphomas of these mice as well as in the spleens and thymuses. The origin of the lymphomas from B- and T-cell lineages suggests that the LPV early genes are expressed in and can transform both of these cell types in vivo.
Topics: Animals; Blotting, Southern; Cell Transformation, Viral; Cerebral Ventricle Neoplasms; Choroid Plexus; Gene Expression Regulation; Genes, Viral; Lymph Nodes; Lymphoproliferative Disorders; Mice; Mice, Transgenic; Neoplasms, Experimental; Papillomaviridae; Pedigree; Polyomaviridae; RNA, Viral; Tissue Distribution
PubMed: 2704077
DOI: 10.1128/JVI.63.5.2204-2214.1989 -
Proceedings of the National Academy of... Jul 1992We have shown that E1 and E2 proteins of human papillomavirus type 11 (HPV-11) were essential to support the replication of the homologous viral origin (ori) in a...
We have shown that E1 and E2 proteins of human papillomavirus type 11 (HPV-11) were essential to support the replication of the homologous viral origin (ori) in a transient replication assay, similar to reports on bovine papillomavirus type 1 (BPV-1). Unexpectedly, matched or even mixed combinations of E1 and E2 proteins from HPV-11 or BPV-1 replicated either ori in human, monkey, and rodent cell lines of epithelial or fibroblastic lineage, albeit with varied efficiencies. Either set of viral proteins was also able to initiate replication of ori-containing plasmids from many other human and animal papillomaviruses. Thus the interactions among the cis elements and trans factors of papillomaviruses are more conserved than expected from the other members of the papovavirus family, simian virus 40 and polyomavirus, for which large tumor antigen does not replicate a heterologous ori in either permissive or nonpermissive cells. We infer that the stringent species and tissue specificities observed for papillomaviruses in vivo are not entirely due to direct restrictions on viral DNA replication. Rather, transcriptional control of viral gene expression must play a dominant role.
Topics: 3T3 Cells; Animals; Base Sequence; Chlorocebus aethiops; Cloning, Molecular; DNA Replication; DNA, Viral; DNA-Binding Proteins; Humans; In Vitro Techniques; Mice; Molecular Sequence Data; Oncogene Proteins, Viral; Papillomaviridae; Regulatory Sequences, Nucleic Acid; Species Specificity; Tumor Cells, Cultured; Viral Proteins; Virus Replication
PubMed: 1321423
DOI: 10.1073/pnas.89.13.5799 -
Infection and Immunity Nov 1982Human papovavirus JC, previously passaged in amnion cells or in primary human fetal glial cells, replicated efficiently in urine-derived epithelial cells. Primary...
Human papovavirus JC, previously passaged in amnion cells or in primary human fetal glial cells, replicated efficiently in urine-derived epithelial cells. Primary isolation of the virus from brain extracts was possible in urine-derived cells, but these cells were not as sensitive as primary human fetal glial cells for this purpose. Primary isolations of human papovavirus JC from urine sediments of renal transplant patients were made in urine-derived cells.
Topics: Cells, Cultured; Epithelial Cells; Humans; JC Virus; Neuroglia; Polyomavirus; Urine; Virus Cultivation; Virus Replication
PubMed: 6292111
DOI: 10.1128/iai.38.2.774-777.1982 -
Journal of Virology May 2000Small DNA tumor viruses like human papillomaviruses, simian virus 40, and adenoviruses modulate the activity of cellular tumor suppressor proteins p53 and/or pRB. These...
Small DNA tumor viruses like human papillomaviruses, simian virus 40, and adenoviruses modulate the activity of cellular tumor suppressor proteins p53 and/or pRB. These viruses replicate as nuclear multicopy extrachromosomal elements during the S phase of the cell cycle, and it has been suggested that inactivation of p53 and pRb is necessary for directing the cells to the S phase. Mouse polyomavirus (Py), however, modulates only the pRB protein activity without any obvious interference with the action of p53. We show here that Py replication was not suppressed by the p53 protein indeed in all tested different mouse cell lines. In addition, E1- and E2-dependent papillomavirus origin replication was insensitive to the action of p53 in mouse cells. We show that in hamster (Chinese hamster ovary) or human (osteosarcoma 143) cell lines the replication of both Py and papillomavirus origins was efficiently blocked by p53. The block of Py replication in human and hamster cells is not caused by the downregulation of large T-antigen expression. The deletion analysis of the p53 protein shows that the RPA binding, proline-rich regulatory, DNA-binding, and oligomerization domains are necessary for p53 action in both replication systems. These results indicate that in mouse cells the p53 protein could be inactive for the suppression of papovavirus replication.
Topics: Animals; Bovine papillomavirus 1; CHO Cells; Cell Line; Cricetinae; Fibroblasts; Gene Expression Regulation, Viral; Humans; Immunoblotting; Mice; Plasmids; Polyomavirus; Polyomavirus Infections; Replication Origin; Transfection; Tumor Cells, Cultured; Tumor Suppressor Protein p53; Tumor Virus Infections; Virus Replication
PubMed: 10775606
DOI: 10.1128/jvi.74.10.4688-4697.2000 -
Journal of Virology Nov 1980Tau antigens (also known as cellular or nonviral tumor antigens) were detected in uninfected and simian virus 40-infected monkey cells after immunoprecipitation with... (Comparative Study)
Comparative Study
Tau antigens (also known as cellular or nonviral tumor antigens) were detected in uninfected and simian virus 40-infected monkey cells after immunoprecipitation with serum from hamsters bearing simian virus 40-induced tumours (anti-T serum). These two proteins (56,000 daltons) were digested to similarly sized peptides with various amounts of Staphylococcus aureus V8 protease. The Tau antigen isolated from infected monkey cells was closely related but was not identical to the corresponding protein from human cells transformed by simian virus 40, as determined by two-dimensional mapping of their methionine-labeled tryptic peptides. Hamster cells transformed by various primate papovaviruses (simian virus 40, BK virus, and JC virus) synthesized indistinguishable Tau antigens, as determined by two-dimensional peptide mapping. When tested by the same procedure, these proteins and the ones made in monkey and human cells were found to be related to the Tau antigens isolated from simian virus 40-transformed mouse and rat cells. Based on these results, an "evolutionary tree" was constructed to show the relationship among the methionine-containing tryptic peptides of all of these proteins.
Topics: Animals; Antigens, Neoplasm; BK Virus; Biological Evolution; Cell Line; Cell Transformation, Viral; Chlorocebus aethiops; Cricetinae; Humans; Mice; Papillomaviridae; Peptides; Polyomaviridae; Rats; Simian virus 40; Species Specificity
PubMed: 6253675
DOI: 10.1128/JVI.36.2.519-525.1980 -
Biophysical Journal Dec 1991The structures of bovine papillomavirus type 1 (BPV-1) and human papillomavirus type 1 (HPV-1) were determined at 2.5 nm resolution by cryoelectron microscopy and three... (Comparative Study)
Comparative Study
The structures of bovine papillomavirus type 1 (BPV-1) and human papillomavirus type 1 (HPV-1) were determined at 2.5 nm resolution by cryoelectron microscopy and three dimensional image reconstruction techniques. As expected, the reconstructions showed that both viruses consist of a T = 7 icosahedral capsid (approximately 60 nm in diameter) which surrounds a nucleohistone core. The capsid morphologies of the two viruses are nearly indistinguishable. Each capsid consists of a shell layer (approximately 2 nm thick) of nearly continuous density from which capsomers project radially to a maximum height of approximately 5.8 nm. The five-coordinate (pentavalent) and six-coordinate (hexavalent) capsomers both exhibit distinct five-fold axial symmetry as was observed for SV40 and polyoma viruses. Thus, both genera (papilloma and polyoma) of the papovavirus family have now been shown to have the characteristic "all-pentamer" capsid construction. BPV-1 and HPV-1 capsomers consist of a thick (8.6 nm diameter) trunk that broadens distally to form a regular five-pointed, star-shaped head, and proximally to create the shell layer where capsomers associate. A cylindrical channel (approximately 2.8 nm diameter) extends along the axis of each capsomer from the interior of the virus to a point approximately half way to the capsomer surface. Computationally sectioned views of individual capsomers displayed at decreasing radii show that each of the five capsomer subunits (in both pentavalent and hexavalent capsomers) makes a pronounced (30 degrees) left-handed twist just above the outer surface of the capsid shell. Similar views of the reconstructions also clarify the morphology of intercapsomer contacts. For example, they show how hexavalent capsomers coordinate six neighboring capsomers despite the fact that they contain only five subunits. The system of intercapsomer contacts is indistinguishable in BPV-1 and HPV-1, but quite different from that reported for polyoma virus capsids assembled in vitro from the major capsid protein, VP1 (D. M. Salunke, D. L. D. Caspar, and R. L. Garcea. 1989. Biophys. J. 56:887-900). Thus, because both polyoma and papilloma viruses have all-pentamer capsids, it appears that intracapsomer subunit-subunit interactions which stabilize pentameric capsomers are better preserved evolutionarily than those involved in capsomer-capsomer contacts.
Topics: Animals; Bovine papillomavirus 1; Cattle; Cattle Diseases; Freezing; Humans; Microscopy, Electron; Models, Structural; Papillomaviridae; Tumor Virus Infections; Warts
PubMed: 1663794
DOI: 10.1016/S0006-3495(91)82181-6 -
Journal of Virology Apr 1984Hamster embryo cells were transformed by African green monkey lymphotropic papovavirus (LPV). The transformed cells contained intranuclear T-antigens demonstrable by...
Hamster embryo cells were transformed by African green monkey lymphotropic papovavirus (LPV). The transformed cells contained intranuclear T-antigens demonstrable by fluorescent antibody staining with hamster anti-LPV serum. Analysis of uncloned and cloned lines of transformed cells for LPV sequences revealed that the viral DNA was present as free nonintegrated and integrated genomes; there were approximately 10 copies of free DNA and about one to two copies of integrated genomes per cell. The cells were highly tumorigenic when inoculated into hamsters and produced progressively growing tumors in 100% of newborn or 10-day-old hamsters that were inoculated with LPV-transformed cells. The serum from tumor-bearing hamsters reacted with LPV-transformed cells and also showed a weak reaction with simian virus 40-, BK virus-, and JC virus-transformed cells, thereby showing an antigenic relationship with the T-antigens of other primate polyomaviruses. The large T-antigen of LPV was found to be an 84,000-molecular-weight protein which was immunoprecipitated by hamster anti-LPV (antiviral) as well as by tumor serum.
Topics: Agar; Animals; Antigens, Viral, Tumor; Blood; Cell Division; Cell Line; Cell Transformation, Neoplastic; Cell Transformation, Viral; Clone Cells; Cricetinae; Culture Media; DNA, Viral; Embryo, Mammalian; Neoplasms, Experimental; Polyomavirus; Tumor Virus Infections
PubMed: 6321782
DOI: 10.1128/JVI.50.1.100-105.1984 -
Journal of Virology Sep 1988The human papovavirus BK has a noncoding regulatory region located between the divergently transcribed early and late coding regions. Many strains of BK virus (BKV) have...
The human papovavirus BK has a noncoding regulatory region located between the divergently transcribed early and late coding regions. Many strains of BK virus (BKV) have direct DNA sequence repeats in the regulatory region, although the number and extent of these repeats varies widely between independent isolates. Until recently, little was known about the individual functional elements within the BKV regulatory region, and the biological significance of the variable repeat structure has been unclear. To characterize the interaction between sequences in the BKV regulatory region and host cell transcription factors, we have carried out DNase I footprinting and competitive binding experiments on three strains of BKV, including one strain that does not contain direct sequence repeats. We have used relatively crude fractions from HeLa cell nuclear extracts, as well as DNA affinity-purified preparations of proteins. Our results demonstrate that BK(Dunlop), BK(WW), and BK(MM) each contain multiple binding sites for a factor, NF-BK, that is a member of the nuclear factor 1 family of transcription factors. We predict the presence of three to eight binding sites for NF-BK in the other strains of BKV for which a DNA sequence is available. This suggests that the binding of this protein is likely to be required for biological activity of the virus. In addition to NF-BK sites, BK(WW) and BK(MM) each contain a single binding site for transcription factor Sp1, and BK(Dunlop) contains two binding sites for transcription factor AP-1. The AP-1 sites in BK(Dunlop) span the junction of adjacent direct repeats, suggesting that repeat formation may be an important mechanism for de novo formation of binding sites not present in a parental strain.
Topics: BK Virus; Binding, Competitive; CCAAT-Enhancer-Binding Proteins; Chromatography, Affinity; DNA, Viral; DNA-Binding Proteins; Deoxyribonuclease I; HeLa Cells; Humans; NFI Transcription Factors; Nuclear Proteins; Polyomavirus; Regulatory Sequences, Nucleic Acid; Repetitive Sequences, Nucleic Acid; Transcription Factors; Y-Box-Binding Protein 1
PubMed: 2841492
DOI: 10.1128/JVI.62.9.3388-3398.1988