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La Lutte Contre Le Cancer 1964
Topics: Animals; Avian Sarcoma Viruses; Bacteriophages; Leukemia Virus, Murine; Mice; Oncogenic Viruses; Papillomaviridae; Polyomavirus; RNA; RNA, Viral; Rous sarcoma virus; Tissue Culture Techniques; Virus Cultivation; Viruses
PubMed: 14224075
DOI: No ID Found -
La Presse Medicale Jan 1968
Topics: Animals; Avian Sarcoma Viruses; Humans; Mice; Oncogenic Viruses; Polyomavirus; Simian virus 40
PubMed: 4295513
DOI: No ID Found -
Virologie 1982Some viewpoints are presented as regards the virus-host cell relationship within the framework of carcinogenesis. Data are reviewed which point out the possibility of...
Some viewpoints are presented as regards the virus-host cell relationship within the framework of carcinogenesis. Data are reviewed which point out the possibility of the transfer of cellular antigenic fractions from the tumor cell to the virus that grows in it, as well as of a hybridization between the virus genome and the genome of the tumoral host cell. Such a hybridization may have multiple consequences, among which the appearance of new oncogenic variants of viruses so far known to be nononcogenic ones.
Topics: Animals; Antibodies, Viral; Genes, Viral; Humans; Oncogenic Viruses; Tumor Virus Infections
PubMed: 7072151
DOI: No ID Found -
Annual Review of Pharmacology 1969
Review
Topics: AKR murine leukemia virus; Animals; Antineoplastic Agents; Anura; Avian Sarcoma Viruses; Biological Products; Cats; Cattle; Cricetinae; Dogs; Friend murine leukemia virus; Guinea Pigs; Haplorhini; Immunity, Maternally-Acquired; Interferons; Mice; Moloney murine leukemia virus; Neoplasms; Oncogenic Viruses; Rabbits; Rats; Rauscher Virus; Vaccines; Viral Interference
PubMed: 4307021
DOI: 10.1146/annurev.pa.09.040169.002243 -
Reviews in Medical Virology 2008
Topics: Animals; Gammaretrovirus; Humans; Male; Mice; Oncogenic Viruses; Polyomavirus; Polyomavirus Infections; Prostatic Neoplasms; Retroviridae Infections; Tumor Virus Infections
PubMed: 18937272
DOI: 10.1002/rmv.596 -
Nature Reviews. Cancer Dec 2012The role of cell polarity regulators in the development of cancer has long been an enigma. Despite displaying characteristics of tumour suppressors, the core regulators... (Review)
Review
The role of cell polarity regulators in the development of cancer has long been an enigma. Despite displaying characteristics of tumour suppressors, the core regulators of polarity are rarely mutated in tumours and there are few data from animal models to suggest that they directly contribute to cancer susceptibility, thus questioning their relevance to human carcinogenesis. However, a body of data from human tumour viruses is now providing compelling evidence of a central role for the perturbation of cell polarity in the development of cancer.
Topics: Alphapapillomavirus; Cell Polarity; Hepatitis Viruses; Herpesviridae; Host-Pathogen Interactions; Human T-lymphotropic virus 1; Human papillomavirus 6; Humans; Merkel cell polyomavirus; Neoplasms; Oncogenic Viruses
PubMed: 23175122
DOI: 10.1038/nrc3400 -
The Journal of Experimental Medicine Aug 1979Murine teratocarcinoma stem cells are nonpermissive for productive infection by a variety of DNA (polyoma and SV40 virus) and RNA (murine leukemia and sarcoma virus)...
Murine teratocarcinoma stem cells are nonpermissive for productive infection by a variety of DNA (polyoma and SV40 virus) and RNA (murine leukemia and sarcoma virus) tumor viruses whereas differentiated murine cells derived from the stem cells are permissive for productive (or abortive in the case of SV40) infection by these same viruses. The block to productive infection by these oncogenic viruses is at a postpenetration step in the replication cycle of these viruses but the precise level of the block has not been established for any of these viruses. In this report we describe teratocarcinoma-derived stem and differentiated cell lines which should be especially useful in determining the level of the block to replication of ecotropic murine leukemia virus in murine teratocarcinoma stem cells. The stem cell line, OTT6050AF1 BrdU, which is completely nonpermissive to productive infection by Moloney murine leukemia virus and consists of 97% pluripotent stem cells, contains DNA copies of an RNA tumor virus which is indistinguishable from the N-tropic murine leukemia virus of AKR mice. The stem cells are negative for expression of viral reverse transcriptase, p30 and gp69/71 and no virus is found by XC plaque assay or other biological tests. Differentiated cells established from the same teratocarcinoma tumor are 100% positive for viral gp69/71, p30, and produce large amounts of reverse transcriptase activity and N-tropic virus as detected by biological assay. The virus isolated from the differentiated cells is closely related, if not identical to AKR N-tropic virus by nucleic acid hybridization studies and is thus not an endogenous virus of the 129 strain of mice. The teratocarcinoma tumor from which the cell lines were established had been carried in 129 mice and perhaps at some time in the mouse passage history the tumors were infected (nonproductively) with the N-tropic virus. Regardless of the origin of this viral DNA, the OTT6050A derived stem and differentiated cell lines should be extremely useful in defining in stem cells the step at which ecotropic murine leukemia virus replication is blocked.
Topics: Animals; Antigens, Neoplasm; Antigens, Viral; Cell Line; Genes, Viral; Mice; Neoplasms, Experimental; Nucleic Acid Hybridization; Oncogenic Viruses; Teratoma
PubMed: 458380
DOI: 10.1084/jem.150.2.392 -
Virology Journal Dec 2016Enzootic nasal tumor virus (ENTV-1) is an ovine betaretrovirus that has been linked to enzootic nasal adenocarcinoma (ENA), a contagious tumor of the ethmoid turbinates...
BACKGROUND
Enzootic nasal tumor virus (ENTV-1) is an ovine betaretrovirus that has been linked to enzootic nasal adenocarcinoma (ENA), a contagious tumor of the ethmoid turbinates of sheep. Transmission experiments performed using virus isolated from cell free nasal tumor homogenates suggest that ENTV-1 is the causative agent of ENA; however, this etiological relationship has not been conclusively proven due to the fact that the virus cannot be propagated in vitro nor is there an infectious molecular clone of the virus.
METHODS
Here we report construction of a molecular clone of ENTV-1 and demonstrate that transfection of this molecular clone into HEK 293T cells produces mature virus particles.
RESULTS
Analysis of recombinant virus particles derived from the initial molecular clone revealed a defect in the proteolytic processing of Gag; however, this defect could be corrected by co-expression of the Gag-Pro-Pol polyprotein from the highly related Jaagsiekte sheep retrovirus (JSRV) suggesting that the polyprotein cleavage sites in the ENTV-1 molecular clone were functional. Mutagenesis of the molecular clone to correct amino acid variants identified within the pro gene did not restore proteolytic processing; whereas deletion of one proline residue from a polyproline tract located in variable region 1 (VR1) of the matrix resulted in production of CA protein of the mature (cleaved) size strongly suggesting that normal virion morphogenesis and polyprotein cleavage took place. Finally, electron microscopy revealed the presence of spherical virus particles with an eccentric capsid and an average diameter of about 100 nm.
CONCLUSION
In summary, we have constructed the first molecular clone of ENTV-1 from which mature virus particles can be produced. Future experiments using virus produced from this molecular clone can now be conducted to fulfill Koch's postulates and demonstrate that ENTV-1 is necessary and sufficient to induce ENA in sheep.
Topics: Animals; Betaretrovirus; Cell Line; Cloning, Molecular; DNA Mutational Analysis; Epithelial Cells; Humans; Microscopy, Electron, Transmission; Oncogenic Viruses; Polyproteins; Protein Processing, Post-Translational; Reverse Genetics; Sheep; Transfection; Viral Proteins; Virion; Virus Replication
PubMed: 28038674
DOI: 10.1186/s12985-016-0660-x -
Water Research Oct 2017Recent studies documented the detection of viruses strongly associated with human cancer in urban sewages and other water environments worldwide. The aim of this study...
Recent studies documented the detection of viruses strongly associated with human cancer in urban sewages and other water environments worldwide. The aim of this study was to estimate the occurrence of human oncogenic viruses in environmental samples (sewage, river, marine, and pool/spa water) using highly sensitive and specific multiplex bead-based assays (Luminex technology). A total of 33 samples were analysed for 140 oncogenic viral agents, including mucosal and cutaneous human papillomaviruses (HPVs), human polyomaviruses (HPyV), human herpesviruses (HHV) and mouse mammary tumour virus (MMTV). Eighty-eight percent of the samples tested positive for at least one viral pathogen and the simultaneous presence of more than one virus was frequent (mean number of positivities/sample = 3.03). A total of 30 different Alpha, Beta and Gamma HPVs were detected, including mucosal and cutaneous types. The high-risk type HPV16 was the most frequently detected virus, identified in 73% of the samples. Of the 12 HPyVs tested, only two (BKPyV and MCPyV) were detected. At least one of these two was present in 48% of the samples. MMTV was detected in 21% of the samples, while herpesviruses - HHV-6 and HHV-1 - were detected in two samples (6%). The present study is the first to provide a comprehensive picture of the occurrence of oncogenic viruses belonging to different families and species in diverse water environments, and the first to successfully use, in environmental samples, a Luminex-based multiplex platform for high throughput screening of infectious agents. Our findings, showing that oncogenic viruses are ubiquitous in water environments, pave the way for future studies on the fate of these pathogens in water environments as well as on their potential for transmission via the waterborne route.
Topics: Animals; Environmental Monitoring; Humans; Oncogenic Viruses; Papillomaviridae; Polyomavirus; Rivers; Sewage
PubMed: 28704770
DOI: 10.1016/j.watres.2017.06.088 -
MBio Aug 2021The methylation of RNA at the N6 position of adenosine (mA) orchestrates multiple biological processes to control development, differentiation, and cell cycle, as well...
The methylation of RNA at the N6 position of adenosine (mA) orchestrates multiple biological processes to control development, differentiation, and cell cycle, as well as various aspects of the virus life cycle. How the mA RNA modification pathway is regulated to finely tune these processes remains poorly understood. Here, we discovered the mA reader YTHDF2 as a caspase substrate via proteome-wide prediction, followed by and validations. We further demonstrated that cleavage-resistant YTHDF2 blocks, while cleavage-mimicking YTHDF2 fragments promote, the replication of a common human oncogenic virus, Epstein-Barr virus (EBV). Intriguingly, our study revealed a feedback regulation between YTHDF2 and caspase-8 via mA modification of mRNA and YTHDF2 cleavage during EBV replication. Further, we discovered that caspases cleave multiple components within the mA RNA modification pathway to benefit EBV replication. Our study establishes that caspase disarming of the mA RNA modification machinery fosters EBV replication. The discovery of an -methyladenosine (mA) RNA modification pathway has fundamentally altered our understanding of the central dogma of molecular biology. This pathway is controlled by methyltransferases (writers), demethylases (erasers), and specific mA binding proteins (readers). Emerging studies have linked the mA RNA modification pathway to the life cycle of various viruses. However, very little is known regarding how this pathway is subverted to benefit viral replication. In this study, we established an unexpected linkage between cellular caspases and the mA modification pathway, which is critical to drive the reactivation of a common tumor virus, Epstein-Barr virus (EBV).
Topics: Adenosine; Caspases; Cell Line; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Humans; Methylation; Oncogenic Viruses; RNA Processing, Post-Transcriptional; RNA, Messenger; Virus Replication
PubMed: 34425696
DOI: 10.1128/mBio.01706-21