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.
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Author Topic: CDC Admits 30 Million
Possibly at Risk For Cancer Due To Polio Vaccine SV40 (Read 7929
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