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Polyoma Cancer Virus Research

Reduction in the overall cancer death rates has resulted in the avoidance of about 650,000 deaths from cancer between 1990 and 2005. Although progress has been made to reduce incidence,mortality rates, and improve survival, cancer still accounts for more deaths than heart disease in persons younger than 85 years of age. PMID: 19474385

Researchers at the University of Ferrara, Italy, state that that aninfectious monkey virus was released to the US public between 1955 and 1963 through contaminated polio vaccines. Transmission vectors also include:

• blood transfusions
• sexual contact
• adolescent and adult stool and urine

The polyoma virus isnot transmitted from mother to child.

Simian Virus 40 Infection in Humans and Association with Human Diseases: Results and Hypotheses.

Virology Journal 2004 January - Barbanti-Brodano G, Sabbioni S, Martini F, Negrini M, Corallini A, Tognon M. Department of Experimental and Diagnostic Medicine, Section of Microbiology, Center of Biotechnology, University of Ferrara, Italy.

Simian virus 40 (SV40) is a monkey virus that was introduced in the human population by contaminated poliovaccines, produced in SV40-infected monkey cells, between 1955 and 1963. Epidemiological evidence now suggests that SV40 may be contagiously transmitted in humans by horizontal infection, independent of the earlier administration of SV40-contaminated poliovaccines. This evidence includes detection of SV40 DNA sequences in human tissues and of SV40 antibodies in human sera, as well as rescue of infectious SV40 from a human tumor. Detection of SV40 DNA sequences in blood and sperm and of SV40 virions in sewage points to the hematic, sexual, and orofecal routes as means of virus transmission in humans. The site of latent infection in humans is not known, but the presence of SV40 in urine suggests the kidney as a possible site of latency, as it occurs in the natural monkey host. SV40 in humans is associated with inflammatory kidney diseases and with specific tumor types: mesothelioma, lymphoma, brain, and bone. These human tumors correspond to the neoplasms that are induced by SV40 experimental inoculation in rodents and by generation of transgenic mice with the SV40 early region gene directed by its own early promoter-enhancer. The mechanisms of SV40 tumorigenesis in humans are related to the properties of the two viral oncoproteins, the large T antigen (Tag) and the small t antigen (tag). Tag acts mainly by blocking the functions of p53 and RB tumor suppressor proteins, as well as by inducing chromosomal aberrations in the host cell. These chromosome alterations may hit genes important in oncogenesis and generate genetic instability in tumor cells. The clastogenic activity of Tag, which fixes the chromosome damage in the infected cells, may explain the low viral load in SV40-positive human tumors and the observation that Tag is expressed only in a fraction of tumor cells. "Hit and run" seems the most plausible mechanism to support this situation. The small tag, like large Tag, displays several functions, but its principal role in transformation is to bind the protein phosphatase PP2A. This leads to constitutive activation of the Wnt pathway, resulting in continuous cell proliferation. The possibility that SV40 is implicated as a cofactor in the etiology of some human tumors has stimulated the preparation of a vaccine against the large Tag. Such a vaccine may represent in the future a useful immunoprophylactic and immunotherapeutic intervention against human tumors associated with SV40. PMID: 15015494

Cellular Entry of Polyoma Viruses

Microbiology Immunology, 2010 April- Tsai B, Qian M.Department of Cell and Developmental Biology, University of Michigan Medical School

Polyoma virusesare nonenveloped DNA tumor viruses that include the murine polyoma virus (mPy), simian virus 40 (SV40), and the human BK, JC, KI, WU, and Merkel Cell viruses. To cause infection, Polyoma viruses must enter host cells and navigate through various intracellular compartments, where they undergo sequential conformational changes enabling them to uncoat and deliver the DNA genome into the nucleus. The ensuing transcription and replication of the genome leads to lytic infection or cell transformation. In recent years, a more coherent understanding of how Polyoma viruses are transported from the plasma membrane to the nucleus is starting to emerge. This review will focus on the decisive steps of Py entry, including engagement of the host cell receptor, targeting to the endoplasmic reticulum (ER), penetration across the ER membrane, nuclear entry, and genome release. Strikingly, a number of these steps resemble the intoxication pathway of the AB(5) bacterial toxins. Thus, as Pys and bacterial toxins hijack similar cellular machineries during infection, a general principle appears to guide their entry into host cells. PMID: 20373089

Image: University of Cape Town Health Sciences

Human Polyoma Viruses and Cancer

Advance Cancer Research, 2010 - Gjoerup O, Chang Y.Cancer Virology Program, Hillman Cancer Research Pavilion, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.

Over 50 years of polyoma virus research has produced a wealth of insights into not only general biologic processes in mammalian cells, but also, how conditions can be altered and signaling systems tweaked to produce transformation phenotypes. In the past few years three new members (KIV, WUV, and MCV) have joined two previously known (JCV and BKV) human polyoma viruses. In this review, we present updated information on general virologic features of these polyoma viruses in their natural host, concentrating on the association of MCV with human Merkel cell carcinoma. We further present a discussion on advances made in SV40 as the prototypic model, which has and will continue to inform our understanding about viruses and cancer. PMID: 20399955

Structural Evaluation of New Human Polyoma Viruses Provides Clues to Pathobiology

Trends Microbiology, 2010 February- Johnson EM.Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA , USA.

In the past three years, remarkable discoveries have added three new human polyoma viruses (KI virus (KIV), WU virus (WUV) and Merkel cell virus (MCV)) to a class that previously had only two disease-causing members (BK virus (BKV) and JC virus (JCV)) identified. Two monkey polyoma viruses, simian virus (SV)40 and B-cell lymphotropic polyoma virus (LPV) are also present in humans. KIV and WUV lack the agnoprotein coding sequence and regulatory micro (mi)RNA clusters of BKV, JCV and SV40. MCV lacks the agnoprotein sequence but generates miRNAs. KIV, WUV and MCV are all widespread in humans. Although they have distinctive tissue tropisms, all these viruses are probably acquired in childhood. Of these viruses, only MCV has thus far been strongly linked to cancer. Marshalled evidence from diverse sources implicates MCV as an etiological agent of Merkel cell carcinoma. This review compares the structural features of the new and previously known polyoma viruses, with the aim of identifying approaches to molecular pathology. Copyright © 2010 Elsevier Ltd. All rights reserved. PMID: 20176487

Association of Autism with Polyoma Virus Infection in Postmortem Brains.

Journal Neurovirology, 2010 March- Lintas C, Altieri L, Lombardi F, Sacco R, Persico AM.Laboratory of Molecular Psychiatry and Neurogenetics, University Campus Bio-Medico, Rome, Italy.

Autism is a highly heritable behavioral disorder. Yet, two decades of genetic investigation have unveiled extremely few cases that can be solely explained on the basis of de novo mutations or cytogenetic abnormalities. Vertical viral transmission represents a nongenetic mechanism of disease compatible with high parent-to-offspring transmission and with low rates of disease-specific genetic abnormalities. Vertically transmitted viruses should be found more frequently in the affected tissues of autistic individuals compared to controls. Our initial step was thus to assess by nested polymerase chain reaction (PCR) and DNA sequence analysis the presence of cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV1), herpes simplex virus type 2 (HSV2), human herpes virus 6 (HHV6), BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) in genomic DNA extracted from postmortem temporocortical tissue (Brodmann areas 41/42) belonging to 15 autistic patients and 13 controls. BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% versus 23%, respectively; P < .05). The majority of positives yielded archetypal sequences, whereas six patients and two controls unveiled single-base pair changes in two or more sequenced clones. No association is present with the remaining viruses, which are found in relatively few individuals (N </= 3). Also polyviral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% versus 7.7%, respectively; P = .08). Follow-up studies exploring vertical viral transmission as a possible pathogenetic mechanism in autistic disorder should focus on, but not be limited to, the role of polyoma viruses. PMID: 20345322

Polyomavirus Shedding In The Stool of Healthy Adults.

Journal Clinical Microbioly, 2009 August - Vanchiere JA, Abudayyeh S, Copeland CM, Lu LB, Graham DY, Butel JS.Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA.

We recently reported the frequent detection of polyomaviruses (BK virus [BKV] or simian virus 40 [SV40]) in 46% of stool samples from hospitalized children. In order to determine if adults exhibit fecal shedding of polyomavirus, single stool specimens from healthy adults were evaluated by PCR. Overall, 20 (18.2%) of 110 specimens were positive for human polyomaviruses: 9 with BKV, 9 with JC virus (JCV), 1 with SV40, and 1 with both JCV and SV40. Among the 94 subjects without immune compromise, 17 (18.1%) were excreting polyomaviruses. This shedding frequency in adults was significantly lower than that observed in children (P < 0.001). These findings support the hypothesis that the gastrointestinal tract may be a site of polyomavirus persistence, and they suggest a fecal-oral route of viral transmission. PMID: 19494079

Reactivation of Infectious Simian Virus 40 From Normal Human Tissues.

Journal Neurovirology. 2004 June - Barbanti-Brodano G, Martini F, Corallini A, Lazzarin L, Trabanelli C, Vignocchi B, Calza N, Iaccheri L, Morelli C, Tognon M. Department of Morphology and Embryology, Section of Histology and Embryology, University of Ferrara, Ferrara, Italy.

In this study, 82 DNA samples of simian virus 40 (SV40)-positive human tumors and normal tissues were transfected into SV40-permissive monkey cells. SV40 wild-type strain 776 was reactivated from two DNA samples, derived from peripheral blood mononuclear cells (PBMCs) of a blood donor and from a vulvar tissue. SV40 reactivation was confirmed by obtaining rescue of SV40 from the DNA of the vulvar tissue in a second transfection experiment. This investigation indicates that infectious SV40 is present in normal human tissues and suggests that (i) PBMCs are probably vectors of SV40 to different tissues of the host and (ii) blood and sexual transmission may be routes of SV40 infection in humans, leading to (iii) virus spread in the human population. PMID: 15204925

Latent Human Polyomavirus Infection In Pregnancy: Investigation of Possible Transplacental Transmission.

Boldorini R, Veggiani C, Amoruso E, Allegrini S, Miglio U, Paganotti A, Ribaldone R, Monga G.Scienze Mediche, Facolta di Medicina e Chirurgia, Novara, Italy.

AIMS: The purpose of the study was to investigate the transplacental transmission of the human polyomaviruses JCV and BKV. METHODS: Urine and blood samples from 300 pregnant women underwent cytological analysis to search for 'decoy cells', nested PCR to identify presence and genotype of isolated polyomaviruses, and sequence analysis of the transcription control region. Nested PCR was also used to study the umbilical cord blood of all their newborns. RESULTS: Decoy cells were identified in only one urine sample (1/300; 0.33%); polyomavirus DNA was detected in 80 urine samples (26.6%) corresponding to BKV alone in 28 samples (9.3%), JCV alone in 49 samples (16.3%) and both JCV-BKV in three samples (1%). Blood samples were positive in 17 cases (5.6%), corresponding to BKV alone in 10 (3.3%), and JCV alone in 7 (2.3%). Rearrangements of the transcription control region were found in only one urinary JCV strain, consisting of the insertion of 13 bp at D block, whereas point mutations were identified in 11 BKV and 11 JCV strains detected from urine. Sequence analysis of the BKV strains detected in blood samples revealed a 20 bp insertion of P block (P42-61) in human chromosomes 20 (five cases) and 14 (three cases); two JCV strains had single bp point mutations. The search for polyomavirus DNA in umbilical cord blood samples was always negative. CONCLUSIONS: Polyomavirus DNA was frequently detected in pregnancy, whereas genomic rearrangements were rare, and no evidence of transplacental transmission of polyomavirus was obtained.

60-80% of Adults In The U.S.Infected With Polyoma Virus

The polyoma virus infections are acquired early in childhood, and 60-80% of adults in the U.S. test seropositive for these viruses. The majority of infections are subclinical and lead to viral latency within the kidney. UPMC

40% of the human population excretesJC polyoma virus through its urine. PMID: 18475011

SV40 Cancer Virus - Genetically Modified Organism (GMO)?

Interview with Edward Haslam, author of "Dr. Mary's Monkey"

Contaminated Polio Vaccine

Polio virus vaccine produced in monkey kidney cells were contaminated by SV40 polyoma virus that was inadequately inactivated by formalin, which wasadministered to several million people. The 2 human polyoma species, JC and BK, were isolated from patients with the same initials in 1971.

Human polyoma virus types

• BK virus was isolated from the urine of a person with the intitials "BK" 4 months after renal (kidney) transplantation.
• JC virus The letters "JC" are the initials of a patient with Hodgkin's disease and PML from whose brain the virus was first isolated. The cellular receptor for JCV on glial cells is a serotonin receptor.
• SV40-Simian (monkey) virus, a primate polyoma viruswas discovered in 1960 as a passenger virus in cultures of rhesus monkey cells.

Source:Virology Online