Jaagsiekte Sheep Retrovirus (JSRV): from virus to lung cancer in sheep

Leroux, Caroline; Girard, Nicolas; Cottin, Vincent; Greenland, Timothy; Mornex, Jean‐François; Archer, Fabienne

doi:10.1051/vetres:2006060

Cited by 58 publications

(62 citation statements)

References 89 publications

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“…This finding led to discoveries of an oncogenic papillomavirus in rabbits [23], mouse mammary tumour virus (MMTV) in mice [24], murine leukaemia virus in mice [25] and simian virus 40 in hamsters [26]. Over the past half-century, many other tumour viruses were associated with malignant and non-malignant neoplasias of domestic and wild animals, mostly in poultry, rodents, cats, rodents, ungulates and primates [27,28].…”

Section: Infectious Cancers In Vertebrates (A) Historical Trendmentioning

confidence: 99%

“…Some cancers in domestic animals are caused by viruses from groups that are not known to cause cancer in humans. For example, Jaagsiekte Sheep Retrovirus causes lung cancer in sheep [28]. It is classified within the beta retroviruses, a group for which no virus has been accepted as a cause of human cancer; moreover, no infectious cause of human lung cancer has yet been generally accepted.…”

Section: Infectious Cancers In Vertebrates (A) Historical Trendmentioning

confidence: 99%

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Infection and cancer in multicellular organisms

Ewald

2015

Phil. Trans. R. Soc. B

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Evolutionary considerations suggest that oncogenic infections should be pervasive among animal species. Infection-associated cancers are well documented in humans and domestic animals, less commonly reported in undomesticated captive animals, and rarely documented in nature. In this paper, we review the literature associating infectious agents with cancer to evaluate the reasons for this pattern. Non-malignant infectious neoplasms occur pervasively in multicellular life, but oncogenic progression to malignancy is often uncertain. Evidence from humans and domestic animals shows that non-malignant infectious neoplasms can develop into cancer, although generally with low frequency. Malignant neoplasms could be difficult to find in nature because of a low frequency of oncogenic transformation, short survival after malignancy and reduced survival prior to malignancy. Moreover, the evaluation of malignancy can be ambiguous in nature, because criteria for malignancy may be difficult to apply consistently across species. The information available in the literature therefore does not allow for a definitive assessment of the pervasiveness of infectious cancers in nature, but the presence of infectious neoplasias and knowledge about the progression of benign neoplasias to cancer is consistent with a widespread but largely undetected occurrence.

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Section: Infectious Cancers In Vertebrates (A) Historical Trendmentioning

confidence: 99%

Section: Infectious Cancers In Vertebrates (A) Historical Trendmentioning

confidence: 99%

Infection and cancer in multicellular organisms

Ewald

2015

Phil. Trans. R. Soc. B

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“…Human endogenous retroviruses (HERVs) are vertically transmitted as stable Mendelian genes in the germline of most eukaryotes. They derive from the integration of exogenous, infectiously transmitted retroviruses in the host genomes and are followed by genetic stabilization through accumulation of mutations [4,10]. Under normal circumstances, HERVs are functionally defective or controlled by host factors [9][10][11].…”

Section: Retrovirusesmentioning

confidence: 99%

“…They derive from the integration of exogenous, infectiously transmitted retroviruses in the host genomes and are followed by genetic stabilization through accumulation of mutations [4,10]. Under normal circumstances, HERVs are functionally defective or controlled by host factors [9][10][11]. Several types of HERVs belong to the betaretroviruses and gammaretroviruses genera [4].…”

Section: Retrovirusesmentioning

confidence: 99%

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Tumorigenesis related to retroviral infections

Braoudaki

Tzortzatou‐Stathopoulou

2011

J Infect Dev Ctries

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Retroviral infections are considered important risk factors for cancer development in humans since approximately 15-20% of cancer worldwide is caused by an infectious agent. This report discusses the most established oncogenic retroviruses, including human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV-1 and -2), Rous sarcoma virus (RSV), Abelson murine leukemia virus (A-MuLV), Moloney murine leukemia virus (M-MuLV), murine mammary tumor virus (MMTV), bovine leukemia virus, (BLV), Jaagsiekte sheep retrovirus (JSRV), and Friend spleen focus-forming virus (SFFV). The role of retroviruses as inducers of carcinogenesis, the mechanisms underlying oncogenic transformation, and the routes of transmission of several cancer-related retroviral infections are also described. Finally, the impact of cancer-related retroviral infections in the developing world is addressed. This review is an update of carcinogenesis caused by retroviral infections.

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A self-encoded capsid derivative restricts Ty1 retrotransposition in Saccharomyces

Garfinkel¹,

Tucker²,

Saha³

et al. 2015

Curr Genet

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Retrotransposons and retroviral insertions have molded the genomes of many eukaryotes. Since retroelements transpose via an RNA intermediate, the additive nature of the replication cycle can result in massive increases in copy number if left unchecked. Host organisms have countered with several defense systems, including domestication of retroelement genes that now act as restriction factors to minimize propagation. We discovered a novel truncated form of the Saccharomyces Ty1 retrotransposon capsid protein, dubbed p22 that inhibits virus-like particle (VLP) assembly and function. The p22 restriction factor expands the repertoire of defense proteins targeting the capsid and highlights a novel host-parasite strategy. Instead of inhibiting all transposition by domesticating the restriction gene as a distinct locus, Ty1 and budding yeast may have coevolved a relationship that allows high levels of transposition when Ty1 copy numbers are low and progressively less transposition as copy numbers rise. Here, we offer a perspective on p22 restriction, including its mode of expression, effect on VLP functions, interactions with its target, properties as a nucleic acid chaperone, similarities to other restriction factors, and future directions.

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Jaagsiekte Sheep Retrovirus (JSRV): from virus to lung cancer in sheep

Cited by 58 publications

References 89 publications

Infection and cancer in multicellular organisms

Infection and cancer in multicellular organisms

Tumorigenesis related to retroviral infections

A self-encoded capsid derivative restricts Ty1 retrotransposition in Saccharomyces

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