Research still ongoing!:
SV40 appears to be contagious like HIV plus fecal-oral transmission route
"the haematic [blood], sexual and orofecal routes of transmission are likely to be responsible for SV40 horizontal infection in humans" http://www.bcm.edu/imbs/?PMID=2046Janet S. Butel, Ph.DDistinguished Service Professor and Chair, Department of Molecular Virology & Microbiology
Ph.D., Baylor University College of Medicine
Postdoctoral, Baylor College of Medicine
Research Interests:
The Butel laboratory is interested in polyomavirus pathogenesis of infections and disease, with a primary focus on polyomavirus SV40. Originally isolated from monkeys, SV40 is a small DNA virus that is able to transform cells in culture and induce tumors in rodents.
As a model tumor virus, SV40 has provided many fundamental insights into
the molecular basis of carcinogenesis.
The large tumor antigen (T-ag) of SV40 is the major transforming protein of the virus, responsible for tumor causation in rodents and transformation of many cell types in culture. It is a complex protein that
possesses multiple functions important for replicating the viral DNA and for dysregulating cell cycle control. Sequence analysis of viral isolates has revealed differences in the structure of the noncoding viral regulatory region as well as the existence of a variable region at the C-terminus of T-ag that can classify SV40 strains into genogroups.
We have developed the Syrian golden hamster small animal model to study SV40 pathogenesis of infection and disease. Recent findings include the significant effect of the structure of the viral regulatory region on both oncogenic potential and vertical transmission in vivo. There was no effect on transforming activity in vitro, indicating that
strain-specific factors affect virus–host interactions that are not detectable using cultured cells. The hamster model is being used to
address the effect of SV40 genetic variations on patterns of viral infection that predispose to disease development.
Research in the last several years has
established that authentic SV40 can cause human infections and is associated with certain types of human tumors, including brain tumors and lymphomas.
New findings related to
human infections include the fecal excretion of polyomaviruses by humans, indicating a probable fecal–oral route of transmission; the
detection of SV40 in normal and malignant lymphoid-rich tissues, suggesting that lymphoid cells are important in the pathogenesis of SV40 infections;
and
the variable frequency of SV40-positive lymphomas in two urban populations with different demographics, emphasizing that SV40 infection and disease likely reflect population differences.
Current research includes an analysis of SV40 effects on human lymphocytes and the role of SV40 microRNA in pathogenesis of infections.
Studies of the newly discovered human cancer virus, Merkel cell polyomavirus, are also in progress.
http://www.ncbi.nlm.nih.gov/pubmed/16626024Polyomaviruses and human diseases.
Abstract
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...
http://www.vacfacts.info/scientific-proof-that-the-known-cancer-causing-sv40-virus-a-previous-contaminant-in-the-polio-vaccine-is-obviously-either-contagious-or-the-virus-is-still-in-the-vaccines.htmlScientific proof that the known
cancer causing SV40 virus, a previous contaminant in the polio vaccine, is obviously either
contagious; or the virus is still in the vaccine/s.
...
http://www.biomedcentral.com/content/pdf/1750-9378-2-13.pdfSimian virus 40 in humans...
To date, the prevalence of SV40 infections in humans is not known. Recent studies, based on PCR and serological techniques, indicate that SV40 infection occurs both in children and adults. (i) SV40 DNA sequences have been detected in normal and neoplastic tissues of people either too young (1 to 30 years) or too old (60 to 85 years) to have been vaccinated with SV40-contaminated anti-polio vaccines [19,33,76-81].
This finding may also explain the lack of difference in cancer incidence between individuals vaccinated with SV40-contaminated and SV40-free anti-polio vaccines [82]. (ii) SV40 sequences and Tag were detected in blood and sperm specimens from normal individuals and oncologic patients [80,81,83-88] and in lymphoblastoid cells [32]. These results suggest that PBMCs could be a reservoir and vehicle of SV40 spreading in the tissues of the host and among the individuals. (iii)
SV40 sequences were found in urine and stoole samples, from children and adults [84,89,90], indicating that the haematic, sexual and orofecal routes of transmission are likely to be responsible for SV40 horizontal infection in humans.
http://www.ncbi.nlm.nih.gov/pubmed/23621738Mikrobiyol Bul.
2013 Apr ;47(2):362-81.
[New, newer, newest human polyomaviruses: how far?]....
Due to the known transforming capacity of SV40, it was initially thought that the incidence of cancer could increase following the administration of SV40-contaminated polio vaccines, however advanced studies yielded inconsistent results, without any evidence to conclude whether or not the contaminated polio vaccine caused cancer.
Several studies have reported
the detection of SV40 genome in some of the human tumors, as well as in the clinical samples of healthy subjects.
In addition
SV40 seropositivity was reported in human populations although in low rates (2-10%). These data have raised the possibility that SV40 infects humans and circulates in human populations unrelated to being exposed to the vaccine.
The discovery of the first human polyomaviruses was in 1971 independently from each other, one was BK virus (BKPyV) isolated from the urine sample of a renal transplant patient, and the other was JC virus (JCPyV) isolated from the brain tissue of a patient with progressive multifocal leukoencephalopathy, and both were named after the patients' initials.
BK and JC viruses were the only well-known human polyomaviruses throughout 36 years, however dramatical increase in number of newly identified human polyomaviruses was recorded in the last six years due to the use of sophisticated molecular methods and new-generation sequencing technologies.
In 2007, two new HPyVs were identified independently from nasopharyngeal aspirates of children with acute respiratory tract infections; one was KI (Karolinska Institute) and the other was WU (Washington University) polyomaviruses, named after the initials of institutes which they were first described.
In 2008, the fifth HPyV namely Merkel cell polyomavirus (MCPyV) was isolated from the skin tumor sample of a patient with Merkel cell carcinoma. In 2010, three other novel human polyomaviruses were discovered, two were from skin samples of healthy subjects (HPyV-6 and HPyV-7), and one (Trichodysplasia Spinulosa-associated virus; TSPyV) from keratotic spicule sample of a heart-transplanted patient.
Another new HPyV was identified in 2011 named HPyV-9, from the blood and urine samples of an asymptomatic patient with kidney transplant.
Most recently,
three new HPyVs have been sequentially discovered during the last quarter of 2012. The 10th HPyV (HPyV10) was identified in condyloma samples of an immunocompromised patient with WHIM syndrome (Wart, Hypogammaglobulinemia, Infections, Myelokathexis), 11th virus was isolated from stool sample of a healthy child from Malawi (Malawi polyomavirus; MWPyV), and 12th was described from fecal sample of a diarrheal child from Mexico (Mexico polyomavirus; MXPyV). The whole genome sequence analysis of HPyV10, MWPyV and MXPyV pointed out that they are closely related viruses.
The last novel polyomavirus, namely Saint Louis polyomavirus (STLPyV) has been reported in a study published on February 2013, identified from the stool sample of a healthy child.
Seroepidemiological studies indicated that most of
the novel HPyVs are highly prevalent (average rate: 40-80%) worldwide and likely acquired asymptomatically during childhood, similar to the old ones, BKPyV and JCPyV. However data about HPyV10, MWPyV, MXPyV and STLPyV are not enough as they have been discovered most recently. Similarly,
little is known about the pathogenesis, route of infection and the relationship with clinical diseases of novel HPyVs except
MCPyV and TSPyV which are known to be responsible for Merkel cell carcinoma and trichodysplasia spinulosa, respectively. The expanding repertoire of human polyomaviruses made us think that many others will be uncovered in the future thanking to the advances in molecular methods. In this review, recent developments subjecting new human polyomaviruses have been summarized.