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At least 19 recordsLinked to original sources
PubMed1976

Infectivity, oncogenicity and transforming ability of BK virus and BK virus DNA.

The human papovavirus, BK, appeared weakly oncogenic in newborn hamsters and was able to induce in vitro transformation of rat kidney cells. The infectivity of BK virus DNA was determined by employing the DEAE-dextran method. In human embryonic cells the infectivity was approx. 10(5) p.f.u./mug of DNA. The transforming ability of BK virus in primary rat kidney cells was measured by employing the calcium method and appeared to vary from 1 to 10 foci per mug of DNA.

Animals↗
PubMed1992

BK virus.

BK virus is a human polyoma virus that infects the renal epithelium and remains latent until immunosuppression triggers reactivation. After reactivation, BK virus can be detected in the urine by methods currently available in the clinical laboratory. Correlations can be made between BK viruria and the occurrence of both renal and hepatic pathologies. BK virus is emerging as a significant pathogen in transplant patients. Additionally, the presence of BK virus DNA in primary brain and pancreatic tumors suggests that it may have oncogenic potential. Thus far, attempts to treat BK virus infection have been ineffective, though research has opened new avenues for treatment possibilities. Prevention of BK virus and other latent viral reactivation remains a challenge to viral research.

BK Virus↗
PubMed1975

Occurrence of BK virus and BK virus-specific antibodies in the urine of patients receiving chemotherapy for malignancy.

Urine specimens from 23 children and 9 adults who were undergoing treatment for malignancy as well as urines from 40 normal individuals were concentrated and examined for evidence of papovavirus infection. Papovavirus particles were detected in 6 of 64 urines examined by electron microscopy. Three of the particle-positive urines induced BK virus-specific immunofluorescence after inoculation of WI38 cells, and three isolations of BK virus were made by inoculation of urines from virus-excreting patients into Vero cells. BK virus-specific hemagglutination-inhibiting and immunofluorescence neutralizing antibodies were found in a majority of urines from adult patients, in about a fifth of pediatric patients, and less often in normal urines. Urines of virus-excreting patients generally had antibodies. In indirect fluorescent antibody tests, BK virus-specific antibodies of the immunoglobulin G class were found in five urine specimens from patients; immunoglobulin A antibodies were not detected in any urine. These data suggest that activation of BK virus is related to immunosuppression and not to transplantation itself and that the occurrence of virus-specific antibodies in urine may be indicative of virus multiplication in the urinary tract.

Adolescent↗
PubMed1977

Relationship between the methionine tryptic peptides of simian virus 40 and BK virus tumor antigens.

The monomer form of BK virus (BKV) tumor antigen (T Ag) was immunoprecipitated from extracts of BKV-transformed cells and had a molecular weight of approximately 113,000. This compared with 97,000 for the molecular weight of either BKV or simian virus 40 (SV40) T Ag from lytically infected cells. The SV40 and BKV T Ag's from productively infected cells were compared by examining their methionine-labeled tryptic peptides. Out of a total of 20 SV40-and 21 BKV-specific peptides, there were seven pairs of similar peptides on the basis of ion-exchange chromatography, These coeluting peptides contained approximately 25 to 30% of the total methionine radioactivity. Similar results were obtained when the tryptic peptides of SV40 T Ag from lytically infected cells were compared with those of BKV T Ag from virally transformed cells.

Antigens, Neoplasm↗
PubMed1976

[Human seroepidemiology Polyoma virus BK in Umbria].

A serological study on the antibody level against BK virus in healthy population and respiratory patients in Umbria was performed. Serum samples of 465 healthy people and 155 patients grouped by age, were tested using HAI. 47% of all sera was positive. The epidemiological implications are discussed.

Adolescent↗
PubMed1992

[Detection of BK virus activation in renal and bone marrow transplantation patients using serological and virological methods].

In this study, 10 renal and bone marrow transplant recipients' sera samples taken before and after transplantation and urine samples taken after transplantation were investigated for evidence of reactivation of BK virus, a human polyoma virus. BK virus reactivation was detected in 4 transplant patients serologically by hemagglutination inhibition, ELISA-IgG and ELISA-IgM tests. However we did not succeed to isolate BK virus in Vero cell lines from any urine samples. Only one patient's urine sediment whom serologic reactivation was detected, contained uroepithelial cells with intranuclear inclusion bodies characteristic for BK virus when examined by Giemsa staining.

Adolescent↗
PubMed1979

Comparative analysis of GS and BK virus genomes.

Analysis of heteroduplexing between the genomes of GS virus, a BK-group virus, and the prototype BK virus revealed one region of nonhomology. Further analysis by cleavage of viral DNA with the restriction endonucleases EcoRI, HindIII, and HaeIII revealed that base changes in the GS virus genome spanned 0.6 to 0.7 map unit from the EcoRI site. Large T and small t antigens of GS virus appear to be similar in size to the BK virus antigens.

Antigens, Neoplasm↗
PubMed1975

Malignant transformation of hamster kidney cells by BK virus.

Primary hamster kidney cells were transformed by BK virus, a new human papovavirus. Transformed (HKBK) cell produced BK virus T antigen and induced tumors in hamsters that developed antibodies to BK virus T antigen. BK virus was rescued from HKBK cells by Sendai virus-assisted fusion with permissive cells. One out of six cell lines derived from HKBK cell-induced tumors showed the same characteristics as HKBK cells.

Animals↗
PubMed1978

Ependymomas, malignant tumors of pancreatic islets, and osteosarcomas induced in hamsters by BK virus, a human papovavirus.

BK virus (BKV), a human papovavirus, was inoculated iv into 3-week-old Syrian golden hamsters. Between 2 1/2 and 9 months after inoculation, 82% of the animals developed tumors. The induced neoplasms were ependymoma, carcinoma of the pancreatic islets, osteosarcoma, adenocarcinoma, angiosarcoma, angioma, lymphoma, and seminoma. Hypersecretion of insulin, glucagon, C-peptide, and calcitonin was detected in tumors of pancreatic islets. BKV etiology of tumors was supported by the following evidence: 1) No tumors with BKV-specific markers appeared in animals given injections of buffer, animals inoculated with BKV neutralized by anti-BKV-specific serum, or uninoculated controls; 2) BKV tumor (T) antigen was detected by immunofluorescence and complement fixation tests in tumors of animals inoculated with infectious BKV and in transplanted tumors; 3) antibodies to BKV T-antigen were detected in sera of animals bearing primary or transplanted tumors; 4) BKV could be activated by Sendai virus-mediated fusion of neoplastic cells with susceptible Vero cells; and 5) no endogenous hamster oncornaviruses were found in tumors.

Animals↗
PubMed1992

Antibodies to eukaryotic, including autologous, native DNA are produced during BK virus infection, but not after immunization with non-infectious BK DNA.

The contemporary view concerning the origin of anti-dsDNA antibodies is that eukaryotic dsDNA is not immunogenic. Results presented here, however, show (1) that inoculation of rabbits with BK virus elicits antibodies to eukaryotic, including autologous, dsDNA, (2) that the transition from a non-immunogenic to an immunogenic state of autologous dsDNA depends on productive infection with BK virus, and (3) that inoculation with protein-free circular BK dsDNA initiates both infection in vivo and production of antibodies to autologous dsDNA. Non-infectious linearized BK dsDNA did not elicit any anti-dsDNA antibodies, while the same DNA molecule, when complexed with methylated bovine serum albumin, elicited anti-dsDNA antibodies solely recognizing BK dsDNA. Neither of the two linearized BK dsDNA preparations initiated infection. Using two different techniques, we could demonstrate that two separate sets of anti-dsDNA antibodies were produced during viral infection; one recognizing BK dsDNA, and the other recognizing autologous dsDNA. Thus, in contrast to previous assumptions, autologous dsDNA may be immunogenic. Based on the present results, we propose that autologous dsDNA can be rendered immunogenic through complex formation with viral DNA binding protein(s) such as the structural protein VP1 or the tumour antigen T. Such DNA-protein complexes may bypass a putative T-cell tolerance to autologous dsDNA.

Animals↗
PubMed1978

Isolation of a variant of BK virus with altered restriction endonuclease pattern.

A papovavirus was isolated from the urine of a 24 year old female who underwent bone marrow transplantation after a relapse of acute myeloid leukemia. The virus (JL) resembles BK virus in its antigenic and growth properties, but has a different restriction endonuclease pattern after digestion with the restriction endonucleases Eco R1 and R Hind II + III.

Adult↗
PubMed1978

Minichromosome from BK virus as a template for transcription in vitro.

BK virus DNA can be extracted from virions as a nucleoprotein complex containing about 20 nucleosomes. Transcription of this "minichromosome" with Escherichia coli RNA polymerase indicates that both initiation and elongation of RNA chains are reduced by the presence of nucleosomes. Hybridization analysis of RNA made on the complex shows preferential transcription of one region of BK virus genome. No increase in strand selection is observed with respect to transcription of purified superhelical BK virus DNA.

BK Virus↗
PubMed1979

BK virus DNA: complete nucleotide sequence of a human tumor virus.

The complete DNA sequence of the human papovavirus BK is presented. From the 4963 base-pair sequence of BK virus (MM strain), the amino acid sequence of at least five proteins can be deduced: a T antigen and a t antigen, which share amino terminal peptides; proteins VP2 and VP3, which share 232 amino acids; and protein VP1, whose coding sequence overlaps those for VP2 and VP3 by 113 nucleotides but is read in a different frame. The gene loci and the arrangement of genes are strikingly similar in BK virus and simian virus 40 (SV40). The sequence of the deduced proteins in BK virus shares 73 percent amino acid homology with those in SV40, whereas the DNA sequence of the two viruses shares 70 percent homology, suggesting close evolutionary relationship. However, the repeated DNA sequences in the noncoding regions of these viruses are different.

Antigens, Viral↗
PubMed1992

Role of phospholipids in BK virus infection and haemagglutination.

The role of phospholipids in BK virus infection and haemagglutination was studied by competition binding experiments and by treatment of susceptible cells with phospholipases. Phospholipids extracted from Vero cells and some commercial phospholipids showed an inhibiting activity on both BK virus infectivity and haemagglutination. The treatment of Vero cells with phospholipases affected the binding of BK virus, but the addition of phospholipids to enzyme-treated cells restored their susceptibility to both viral infectivity and haemagglutination.

Animals↗
PubMed1976

Occurrence of BK virus DNA in DNA obtained from certain human tumors.

DNA sequences from BK virus have been detected by measurements of reassociation kinetics in DNA preparations isolated from five of 12 human tumor tissues and three of four human tumor cell lines; no DNA sequences from BK virus could be found using the same assay in DNA samples obtained from nontumor tissues removed from various patients. Whether or not this association is trivial, indicative of infection by BK virus, or correlative with the tumor state must await the testing of additional samples of normal and tumor tissues as well as a definition of the physical state of the genome of BK virus.

Antigens, Viral↗
PubMed1977

Induction of brain tumors in hamsters with BK virus, a human papovavirus.

The oncogenicity of BK virus for the central nervous system was studied in newborn hamsters. The virus was weakly oncogenic after intracerebral inoculation. Two of 45 hamsters treated with antithymocyte serum developed tumors whereas no untreated hamsters developed tumors. Both tumors were choroid plexus papillomas by histologic and electron microscopic examination. Cells cultured from one tumor had growth characteristics of transformed cells and had intranuclear T antigen; but infectious virus could not be rescued. Cultured tumor cells were weakly oncogenic for hamsters, but theoncogenicity of these cells was enhanced when the recipient animals were treated with antithymocyte serum. The possible role of host immune response as a basis for the weak oncogenicity of BK virus is discussed.

Animals↗
PubMed1979

Electron microscopic features of a brain tumor induced in hamster by BK virus, a human papova virus.

In order to locate the target cells for malignant transformation by BK virus (a human papova virus) in hamster brain, electron microscopic observation of tumor originally induced in hamster brain by BK virus was performed. With light microscopy, the BK virus-induced tumor (Vn 17) bore a close resemblance to human malignant ependymoma. Under the electron microscope, numerous microvilli and few cilia were visible on the surface of the tumor cells. These tumor cells were joined to each other by desmosomes. Gap junctions were not observed. Multilayered cuboidal cells were observed around the lumen and blood vessels in the tumor. With regard to fine structure, three types of Vn 17 cells were recognized; ependymal like cells, tanycytes with prominent cell processes, and undifferentiated cells with few cytoplasmic organelles. There was no basal lamina between the ependymal cells and the connective tissue stroma. The Vn 17 cells showed some similarity to the ultrastructural features of the epemdymal cells of newborn rabbits, suggesting that the target cells for Vn 17 may be cells related to ependyma. Malignant transformation of the cells would be initiated in the early stages after BK virus inoculation into the brain of newborn hamsters.

Animals↗