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PubMed1984

Prospective study of the human polyomaviruses BK and JC and cytomegalovirus in renal transplant recipients.

Forty eight renal transplant recipients were investigated prospectively for evidence of infection with the polyomaviruses BK and JC and cytomegalovirus. An active polyomavirus infection was shown in 31 patients (65%) and cytomegalovirus in 30 (62.5%). Half of the BK and JC virus infections occurred within the first three months after transplantation compared with 93% of the cytomegalovirus infections. Very late polyomavirus infections two or more years after the transplant were also shown. Cytology was useful in identifying polyomavirus but not cytomegalovirus infections, and 21 (68%) of the 31 polyomavirus infected patients excreted inclusion-bearing cells. Only three patients had symptoms possibly associated with the polyomavirus infection. One patient with BK virus infection developed ureteric stenosis and a second patient had malaise and vomiting. One patient with JC virus infection developed pericarditis and effusion. Renal function became impaired at the time of the polyomavius infection in eight patients (26%) and ureteric obstruction and pericarditis developed in two patients treated with methyl prednisolone for possible rejection. At the end of the study 25 of the 31 polyomavirus infected patients (81%) had functioning renal grafts. The detection of polyomavirus infection is important as increased immunosuppression needs to be avoided to prevent possible complications such as ureteric stenosis in transplant recipients.

Adolescent↗
PubMed2006

Serological cross reactivity between polyomavirus capsids.

Multiple methods have been used to measure antibodies to polyomavirus virions. In order to have a common method for all polyomaviruses, we developed enzyme immunoassays (EIAs) using virus-like-particles (VLPs) produced in the baculovirus expression system. We tested serum samples from humans and rhesus macaques in VLP-based EIAs for the two human polyomaviruses, BK and JC virus, and two nonhuman primate polyomaviruses, simian virus 40 (SV40) and lymphotropic polyomavirus (LPV). Rhesus sera exhibited low level reactivity to BK and JC, and approximately 10 and 15% of human sera showed low level reactivity to SV40 and LPV, respectively. Competitive inhibition assays with VLP protein demonstrated that the reactivity of rhesus sera against BK and JC VLPs was blocked by both SV40 and the respective human polyomavirus, indicating that the BK and JC assays were detected cross-reacting antibodies. Similarly, the reactivity of the majority of human sera to SV40 was blocked by both SV40 and BK or JC, demonstrating that the SV40 reactivity of human sera is largely due to cross reacting BK and JC antibodies. In contrast, the reactivity of human sera to LPV VLPs was blocked by LPV but not by BK or JC, providing serological evidence for an unknown human polyomavirus related to LPV. SV40 and LPV VLP-based EIAs and competitive inhibition assays with heterologous VLPs provide tools for seroepidemiological studies of possible SV40 and LPV-like infections of humans.

Antibodies, Viral↗
PubMed2000

Development of a blocking enzyme-linked immunosorbent assay for the detection of avian polyomavirus-specific antibodies.

Avian polyomavirus, described originally as budgerigar fledgling disease virus, has been associated with devastating contagious disease outbreaks in budgerigar aviaries. At present, this virus affects a wide range of psittacine and non-psittacine birds worldwide, and the serum neutralisation test is used for the serodiagnosis of avian polyomavirus infections. A blocking enzyme-linked immunosorbent assay was developed for the screening of large numbers of sera collected from various avian species. The assay employs a monoclonal antibody directed against the major structural protein VP1 as a blocking antibody in a sandwich blocking procedure. Either purified avian polyomavirus particles or avian polyomavirus VP1 expressed in recombinant baculovirus-infected Sf9 cells were used as antigen. The specificity of the blocking enzyme-linked immunosorbent assay was evaluated by testing sera directed against mammalian polyomaviruses. Using sera obtained from chicken infected experimentally with avian polyomavirus and a collection of psittacine field-origin sera, a good correlation was observed between the results of the blocking enzyme-linked immunosorbent assay and the serum neutralisation test. However, the blocking enzyme-linked immunosorbent assay is more rapid and more economic. Both, avian polyomavirus particles and VP1 produced by recombinant DNA technology proved to be suitable antigens.

Animals↗
PubMed2001

Polyomavirus BK nephropathy in a kidney transplant recipient: critical issues of diagnosis and management.

Diagnosis of polyomavirus BK nephropathy and treatment by low-dose immunosuppression may be optimized by using surrogate markers, such as the detection of viral inclusion bearing cells in the urine and polyomavirus BK DNA in plasma by polymerase chain reaction. These markers were used prospectively in the management of a 44-year-old woman and led to the diagnosis of polyomavirus BK nephropathy at an early stage. The management was complicated by the concurrence of acute allograft rejection. Two treatment steps were initiated: antirejection therapy consisting of methylprednisolone for 3 days followed by lowering of the maintenance immunosuppression. This treatment resulted in a return of the serum creatinine concentration to the baseline of 1.6 mg/L, clearance of polyomavirus BK from plasma, and disappearance of viral inclusion bearing cells from the urine. After 2 months of stable allograft function, a control biopsy confirmed the resolution of polyomavirus BK nephropathy. Histologic signs of acute interstitial rejection were found and preemptively treated by methylprednisolone without altering the baseline regimen. Allograft function remained stable without evidence of recurrent polyomavirus BK nephropathy. This case shows the value of surrogate markers used in a prospective fashion for diagnosis and management of polyomavirus BK nephropathy with concurrent rejection.

Adult↗
PubMed1984

Construction and functional characterization of polyomavirus genomes that separately encode the three early proteins.

Modified polyomavirus genomes that individually encode the large and small T proteins were constructed by exchanging restriction endonuclease fragments between cDNA copies of the respective mRNAs and cloned genomic DNA. The efficacies of the new constructs, and that of the middle T protein gene described previously (R. Treisman , U. Novak, J. Favaloro , and R. Kamen , Nature [London] 292:595-600, 1981), were demonstrated with simian virus 40 (SV40)-polyomavirus recombinants in which part or all of the SV40 late region was replaced with the modified polyomavirus early genes. Each of the three recombinant viruses induced the synthesis of only the expected polyomavirus early protein in infected CV-1 cells. The rates of synthesis of large, middle, and small T proteins were ca. 1.5, 4.0, and 9.0 times the rate of synthesis of SV40 large T protein, respectively. The deletion of introns had no detrimental effect on mRNA biogenesis. Indeed, a further polyomavirus-SV40 recombinant, containing wild-type polyomavirus early region DNA, expressed an aberrant 58,000-dalton form of the middle T protein which we believe to result from utilization of a cryptic splice site. Immunofluorescence studied with monkey cells infected by the recombinant viruses allowed us to determine the cellular locations of the polyomavirus early proteins. Overproduction of the middle T protein did not result in a corresponding overproduction of the middle T protein-associated tyrosine phosphokinase activity.

Animals↗
PubMed1991

Mouse DNA primase plays the principal role in determination of permissiveness for polyomavirus DNA replication.

We have investigated the species-specific replication of polyomavirus DNA in the cell-free system that was established previously (Y. Murakami, T. Eki, M. Yamada, C. Prives, and J. Hurwitz, Proc. Natl. Acad. Sci. USA 83:6347-6351, 1986). Extracts from various species of cells supported polyomavirus DNA replication in a species-specific manner that was consistent with the host range specificity of polyomavirus; extracts prepared from mouse and hamster cells were active, whereas extracts prepared from human, monkey, and insect cells were inactive. The addition of DNA polymerase alpha-primase purified from mouse cells induced the replication of polyomavirus DNA in a cell-free system containing polyomavirus large tumor antigen and nonpermissive cell extracts, such as human and insect cell extracts. Isolated mouse DNA primase alone also induced polyomavirus DNA replication in human cell extracts but not in insect cell extracts, indicating that mouse DNA primase plays the principal role in determining permissiveness for polyomavirus DNA replication.

Animals↗
PubMed2004

Polyomavirus nephropathy in kidney transplantation.

Polyomavirus nephropathy has become an important complication in kidney transplantation, with a prevalence of 1% to 8%. Unfortunately, the risk factors for polyomavirus nephropathy and renal allograft loss are not well defined. The definitive diagnosis is made through assessment of a kidney transplant biopsy. Recently, noninvasive urine and serum markers have been used to assist in polyomavirus nephropathy diagnosis and monitoring. Primary treatment is immunosuppression reduction, but must be balanced with the risks of rejection. No antiviral treatments for polyomavirus nephropathy have been approved by the Food and Drug Administration. Although cidofovir has shown in vitro activity against murine polyomaviruses, and has been effective in some patients, it is associated with significant nephrotoxicity. Graft loss due to polyomavirus nephropathy should not be a contraindication to retransplantation; however, experience is limited. This review presents potential risk factors, screening, diagnostic and monitoring methods, therapeutic management, and retransplantation experience for polyomavirus nephropathy.

Antiviral Agents↗
PubMed1985

Control of Polyomavirus T-antigen and DNA synthesis in mouse embryo fibroblast cells by vitamin A.

Vitamin A (retinoic acid, 10(-6) M) treatment of confluent mouse embryo cells for only 7 h resulted in optimal inhibition of Polyomavirus replication. Depending upon the input multiplicity of virus, one could wait until between 12 and 18 h postinfection to add vitamin A and still observe maximal inhibition of virus yields. Taken together, and assuming the same kinetics before and after virus infection, these results suggested that the inhibitory action of vitamin A occurred between 19 and 25 h into the Polyomavirus replication cycle. In this model system, such a time corresponded to the onset of T-antigen expression and virus-induced cellular DNA synthesis. Analysis of both viral and virus-induced cellular DNA synthesis by the method of Hirt (J. Mol. Biol., 26: 365-369, 1967) and by cesium chloride gradients suggested that vitamin A preferentially inhibited viral, more than virus-induced cellular, DNA synthesis in confluent cell monolayers. Vitamin A also concomitantly inhibited Polyomavirus T-antigen expression in such confluent cultures. In contrast, viral DNA synthesis and infectious virus yields were not significantly inhibited by vitamin A in subconfluent cell cultures. The antagonistic effect of vitamin A on Polyomavirus replication in confluent monolayers could be blocked with cycloheximide, a reversible protein synthesis inhibitor. This suggested that vitamin A inhibition of Polyomavirus replication was indirect and mediated by a newly synthesized protein. Taken together, these results suggest that vitamin A induced a protein in confluent, but not subconfluent, cells, which blocked the expression of Polyomavirus T-antigen. Decreased amounts of T-antigen most likely reduced Polyomavirus and cellular DNA synthesis and virus yield.

Animals↗
PubMed1986

Cloning and characterization of budgerigar fledgling disease virus, an avian polyomavirus.

The DNA of a virus isolated from fledgling budgerigars, designated BFDV, was cloned and analyzed with regard to its relationship to the polyomavirus subgroup of the papovavirus family. Under relaxed conditions, the DNA of BFDV cross-hybridized with the DNAs of members of the polyomavirus subgroup, such as the mouse polyomavirus, the monkey viruses simian virus 40, stump-tailed macaque virus, and lymphotropic papovavirus, and the human viruses JCV and BKV. Under stringent conditions, however, no homologies could be detected. Furthermore, BFDV propagated in chicken embryo cells was antigenically related to the capsid antigen(s) of the other polyomaviruses. The virus was able to transform hamster embryo cells in vitro which is a typical feature of polyomaviruses. These data clearly indicate that BFDV is a new distinct member of the polyomavirus genus representing the first nonmammalian polyomavirus.

Animals↗
PubMed1980

Activation of human polyomavirus infection-detection by cytologic technics.

Human polyomaviruses produce characteristic large basophilic nuclear inclusions in urothelial cells. Cytologic screening of urinary sediment for inclusion-bearing cells permits the identification of persons who are actively excreting these viruses. The human polyomavirus-induced changes may be differentiated from changes induced by other viruses and from cancer by transmission electron microscopy of infected cells. Cytologic evidence of virus infection was detected in five of 37 cancer patients receiving various treatments, two of whom were also diabetic, and in two of 84 adult patients who had diabetes mellitus. The monitoring of 3,648 urine samples sent for routine cytologic examination revealed 12 additional patients to have cytologic changes of human polyomavirus infection. Electron microscopy confirmed the presence of polyomavirus particles in seven of the 19 cytologically positive specimens. Previous reports of human polyomavirus excretion have been confined to describing patients whose immunity may have been impaired by drug therapy, congenital disease, or pregnancy. This study indicates that cytologic evidence of active human polyomavirus infection may be found among patients receiving various treatments for a number of medical disorders not usually associated with immunologic defects. Further studies to identify factors concerned in the reactivation of human polyomavirus are indicated.

Adult↗
PubMed2005

Detection of polyomavirus BK and JC in children with kidney diseases and renal transplant recipients.

BACKGROUND: Reactivation of polyomavirus is a known reason for severe renal dysfunction in adult renal transplant recipients. Testing for polyomavirus DNA in plasma has been described as a sensitive and specific method to discover viral nephropathy in adult patients. We were now interested in polyomavirus status in a pediatric patient setting. METHODS: Plasma and urine samples were obtained from 80 children including 38 children after renal transplantation (group 1), 7 children with different kidney diseases receiving immunosuppressive treatment (group 2) and 35 children with different kidney diseases not receiving immunosuppressive treatment (group 3). A nested polymerase chain reaction method was used for amplification of polyomavirus DNA fragments. Differentiation between JC and BK virus was done by digestion with restriction endonucleases. RESULTS: Polyomavirus DNA was detected in the urine sample of 19 of 38 (50%) renal transplant recipients (group 1), of 1 of 7 (14%) patients from group 2 and in none of the 35 patients of group 3. Plasma samples from 3 (8%) of group 1 patients and from 1 child each of group 2 (14%) and group 3 (3%) were tested positive for polyomavirus DNA. CONCLUSION: Urinary polyomavirus excretion seems to be more frequent in pediatric patients with kidney diseases receiving immunosuppressive treatment and after renal transplantation than in children with various kidney diseases without immunosuppressive treatment.

Adolescent↗
PubMed1997

Polyomavirus major capsid protein VP1 is capable of packaging cellular DNA when expressed in the baculovirus system.

Using the p2Bac dual multiple cloning site transfer vector, the polyomavirus major capsid protein gene VP1 was cloned for expression in the baculovirus-insect cell expression system. The 5-day-infected cellular lysate from this recombinant preparation was purified by cesium chloride density gradient centrifugation. Capsid-like particles were observed in the resulting preparation. The purified particle preparation was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and was shown to have accurately expressed the polyomavirus VP1 protein as cloned. It was found that the preparation revealed the presence of host histones in the stained gels, which is indicative of DNA packaging. To determine if cellular DNA was being packaged in the particles, Sf9 insect cells were prelabeled with [3H] thymidine. The label was removed, and the cells were subsequently infected with a recombinant Autographa californica multiple nuclear polyhedrosis virus (AcMNPV) carrying the polyomavirus VP1 gene. Upon purification through three cesium chloride gradients and DNase I treatment, capsid-like particles, containing [3H]thymidine-labeled DNA, were isolated which were found to coincide with hemagglutination activity. Studies have indicated that the AcMNPV appears to have the ability to fragment Sf9 cellular DNA. When infected with the recombinant AcMNPV carrying the VP1 gene of polyomavirus, these host DNA fragments are being packaged by the VPI major capsid protein; further, these DNA fragments have been shown to be approximately 5 kb in size, which corresponds to the size of the native polyomavirus genome. These studies demonstrate that the recombinant polyomavirus VP1 protein has the ability to package DNA in the absence of the minor structural proteins VP2 and VP3 and independently of the polyomavirus T antigens.

Animals↗
PubMed1997

Consequences of a subtle sialic acid modification on the murine polyomavirus receptor.

Polyomaviruses are small, nonenveloped DNA tumor viruses with restricted host ranges. Virus binding to cell surface receptors is one determinant of viral tropism. Although murine polyomavirus is among the best characterized viruses, little is known about the sialic acid-containing receptor and its interaction with viral particles. By using nonradioactive virus binding assays as recently described for the B-lymphotropic papovavirus, murine polyomavirus particles were found to bind in a saturable and noncooperative manner to 25,000 receptors per 3T6 mouse fibroblast. The virus-receptor interaction at 4 degrees C was of high affinity (Kd = 1.8 x 10(-11) M), very fast (k1 = 1.7 x 10(7) M(-1) s(-1)), and stable (half-life = 38 min). Elongation of the N-acyl side chain of sialic acid by biosynthetic modulation with synthetic precursor analogs has been shown for other polyomaviruses to influence both sialic acid-dependent binding and infection (O. T. Keppler, P. Stehling, M. Herrmann, H. Kayser, D. Grunow, W. Reutter, and M. Pawlita, J. Biol. Chem. 270:1308-1314, 1995). In 3T6 cells in which about one-third of the sialic acids were modified, infection and binding of polyomavirus particles were significantly reduced. The number of receptors per cell was decreased to 18,000, with the remaining receptors displaying the same affinity as in untreated cells. Molecular modeling studies based on the three-dimensional structure of a mouse polyomavirus-sialyllactose complex recently solved by T. Stehle and coworkers (T. Stehle, Y. W. Yan, T. L. Benjamin, and S. C. Harrison, Nature 369:160-163, 1994) were performed. They suggest that the elongation of the N-acyl side chain by a single methylene group leads to steric hinderence, with the peptide backbone of a loop walling the tip of the shallow sialic acid binding groove. This collision appears to be incompatible with functional binding. The data are taken as a basis to discuss possible features of the organization and topology of the cellular receptor for mouse polyomavirus.

Animals↗
PubMed2005

Lack of association of polyomavirus and herpesvirus types 6 and 7 in human lymphomas.

BACKGROUND: The association of viruses with several human tumors has been studied for almost 100 years, and it remains a very controversial issue. Due to the fact that the presence of polyomaviruses and herpes viruses reportedly are associated with lymphomas, albeit with striking results and differences between the many studies, the authors undertook a study into the presence of viral sequences of polyomavirus (BK virus, JC virus, and especially simian virus 40 [SV40]) in human lymphomas in an attempt to explain this contradictory association. To complete the study, the presence of different virus types from the herpesviriridae family were analyzed, such as herpesvirus type 6 (HHV6), HHV7, HHV8, and Epstein-Barr virus, in human lymphomas. METHODS: DNA was isolated from 83 frozen human lymphoma samples, and different polymerase chain reaction techniques were used to find polyomavirus and herpesvirus sequences in these samples. To assess the incidence of the presence of sequences in lymphomas, a parallel analysis was made of 53 samples from normal donor spleen lymphocytes. Positive samples were analyzed for polyomavirus sequences by immunohistochemistry. RESULTS: Polyomavirus sequences were detected in 9 of 83 lymphomas (11%), and SV40 sequences could be confirmed in only 1 lymphoma. Immunohistochemistry for large-T antigen was negative in all samples. Herpesviruses were detected in 53 of 83 lymphomas (63.9%), were detected more frequently in Hodgkin lymphomas (80%) than in non-Hodgkin lymphomas (58.7%), and were detected in > 60% of normal spleen lymphocytes. CONCLUSIONS: The current results did not support a clear association of polyomavirus and HHV6 or HHV7 with lymphomas; HHV6 and HHV7 sequences were detected in a similar percentage of normal samples and lymphomas. The lack of significant differences between normal and malignant lymphocytes and the absence of viral protein expression in the tumor cells did not allow the establishment of a clinical correlation between polyomaviruses or HHVs (HHV6, HHV7, HHV8) and lymphomas. Nevertheless, because viral products can be lost during tumor progression, and because host factors can modulate the oncogenic role of some viruses, the hypothetical role of these viruses cannot be discarded completely.

Adult↗
PubMed2004

Simultaneous detection and differentiation of human polyomaviruses JC and BK by a rapid and sensitive PCR-ELAHA assay and a survey of the JCV subtypes within an Australian population.

Human polyomaviruses JCV and BKV can cause several clinical manifestations in immunocompromised hosts, including progressive multifocal leukoencephalopathy (PML) and haemorrhagic cystitis. Molecular detection by polymerase chain reaction (PCR) is recognised as a sensitive and specific method for detecting human polyomaviruses in clinical samples. In this study, we developed a PCR assay using a single primer pair to amplify a segment of the VP1 gene of JCV and BKV. An enzyme linked amplicon hybridisation assay (ELAHA) using species-specific biotinylated oligonucleotide probes was used to differentiate between JCV and BKV. This assay (VP1-PCR-ELAHA) was evaluated and compared to a PCR assay targeting the human polyomavirus T antigen gene (pol-PCR). DNA sequencing was used to confirm the polyomavirus species identified by the VP1-PCR-ELAHA and to determine the subtype of each JCV isolate. A total of 297 urine specimens were tested and human polyomavirus was detected in 105 specimens (35.4%) by both PCR assays. The differentiation of JCV and BKV by the VP1-PCR-ELAHA showed good agreement with the results of DNA sequencing. Further, DNA sequencing of the JCV positive specimens showed the most prevalent JCV subtype in our cohort was 2a (27%) followed by 1b (20%), 1a (15%), 2c (14%), 4 (14%) and 2b (10%). The results of this study show that the VP1-PCR-ELAHA is a sensitive, specific and rapid method for detecting and differentiating human polyomaviruses JC and BK and is highly suitable for routine use in the clinical laboratory.

Adolescent↗
PubMed1995

Polyomavirus persists in CD4/8 double-knockout, but not in CD4 or CD8 single-knockout mice.

The effects of incomplete immunocompetence on possible persistence and reactivation of polyomavirus in adult mice were investigated by a polyomavirus-specific polymerase chain reaction (PCR). The presence of virus DNA was followed between 4 days and 2 months postinfection (p.i.) in polyomavirus-infected normal adult A/Sn mice and CD4-/- and CD8-/- single-knockout, as well as CD4-/-8-/- double-knockout BALB/c or C57BL/6 mice. The same study was performed in A/Sn mice immunosuppressed by thymectomy (THX), cytosine-beta-D-arabinofuranoside (Ara-C) treatment, and total body irradiation (TBI). Primary polyomavirus infection of CD4-/- or CD8-/- single-knockout mice was similar to that obtained in normal adult mice when followed by PCR. Viral DNA was detected in a limited number of organs during 4 weeks p.i., but was no longer observed after 1-2 months. In contrast, the virus could be detected in most organs of CD4-/-8-/- double-negative mice and in THX-, Ara-C-, and TBI-treated adult mice and was still present 1-2 months p.i. In polyomavirus-infected normal adult mice a later immunosuppression did not lead to reactivation of the virus. Furthermore, if a second challenge of polyomavirus was administered 4 weeks after primary infection in both normal or recently immunosuppressed mice no viral DNA could be detected by PCR.

Animals↗
PubMed2006

Polyomaviruses and human diseases.

Polyomaviruses are small, nonenveloped DNA viruses, which are widespread in nature. In immunocompetent hosts, the viruses remain latent after primary infection. With few exceptions, illnesses associated with these viruses occur in times of immune compromise, especially in conditions that bring about T cell deficiency. The human polyomaviruses BKV and JCV are known to cause, respectively, hemorrhagic cystitis in recipients of bone marrow transplantation and progressive multifocal leukoencephalopathy in immunocompromised patients, for example, by HIV infection. Recently, transplant nephropathy due to BKV infection has been increasingly recognized as the cause for renal allograft failure. Quantitation of polyomavirus DNA in the blood, cerebrospinal fluid, and urine, identification of virus laden "decoy cells" in urine, and histopathologic demonstration of viral inclusions in the brain parenchyma and renal tubules are the applicable diagnostic methods. Genomic sequences of polyomaviruses have been reported to be associated with various neoplastic disorders and autoimmune conditions. While various antiviral agents have been tried to treat polyomavirus-related illnesses, current management aims at the modification and/or improvement in the hosts' immune status. In this chapter, we provide an overview of polyomaviruses and briefly introduce its association with human diseases, which will be covered extensively in other chapters by experts in the field.

Antiviral Agents↗
PubMed2005

Human polyomaviruses and brain tumors.

Polyomaviruses are DNA tumor viruses with small circular genomes. Three polyomaviruses have captured attention with regard to their potential role in the development of human brain tumors: JC virus (JCV), BK virus (BKV), and simian vacuolating virus 40 (SV40). JCV is a neurotropic polyomavirus that is the etiologic agent of progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the central nervous system occurring mainly in AIDS patients. BKV is the causative agent of polyomavirus-associated nephropathy (PVN) which occurs after renal transplantation when BKV reactivates from a latent state during immunosuppressive therapy to cause allograft failure. SV40, originating in rhesus monkeys, gained notoriety when it entered the human population via contaminated polio vaccines. All three viruses are highly oncogenic when injected into the brain of experimental animals. Reports indicate that these viruses, especially JCV, are associated with brain tumors and other cancers in humans as evidenced from the analysis of clinical samples for the presence of viral DNA sequences and expression of viral proteins. Human polyomaviruses encode three non-capsid regulatory proteins: large T-antigen, small t-antigen, and agnoprotein. These proteins interact with a number of cellular target proteins to exert effects that dysregulate pathways involved in the control of various host cell functions including the cell cycle, DNA repair, and others. In this review, we describe the three polyomaviruses, their abilities to cause brain and other tumors in experimental animals, the evidence for an association with human brain tumors, and the latest findings on the molecular mechanisms of their actions.

Animals↗