MCV and Merkel cell carcinoma: a molecular success story

Arora, Reety; Chang, Yuan; Moore, Patrick S.

doi:10.1016/j.coviro.2012.05.007

Cited by 95 publications

(104 citation statements)

References 98 publications

(145 reference statements)

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“…Little is known about MCPyV targeting of innate immune defenses or the importance of this targeting to viral persistence (39). In this study, we show that MCPyV, similar to the human tumor viruses HBV, EBV, and HPV16, inhibits the expression of TLR9.…”

Section: Discussionmentioning

confidence: 68%

The T Antigen Locus of Merkel Cell Polyomavirus Downregulates Human Toll-Like Receptor 9 Expression

Sattar

Shuda

Gheit

et al. 2013

J Virol

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Section: Discussionmentioning

confidence: 68%

The T Antigen Locus of Merkel Cell Polyomavirus Downregulates Human Toll-Like Receptor 9 Expression

Sattar

Shuda

Gheit

et al. 2013

J Virol

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“…Increased incidence of MCC in immunosuppressed patients has been reported in organ transplant recipients (49) and in HIV patients (5), leading to the hypothesis of an infectious etiology for MCC (1). MCC is a rare tumor caused by a very common viral skin infection as, in addition to loss of immune surveillance, viral integration and LTag deletion and/or mutations eliminating both T antigen replication capacity and expression of highly antigenic major capsid protein are required for MCC cell survival (50).…”

Section: Mcpyv Pathologymentioning

confidence: 99%

Human Merkel cell polyomavirus: virological background and clinical implications

Coursaget

Samimi

Nicol

et al. 2013

APMIS

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The Merkel cell polyomavirus (MCPyV), identified in humans in 2008, is associated with a relatively rare but aggressive neuroendocrine skin cancer, the Merkel cell carcinoma (MCC). MCC incidence is increasing due to the advancing age of the population, the increase in damaging sun exposure and in the number of immunocompromised individuals. MCPyV must be considered as the etiological agent of MCC and thus is the first example of a human oncogenic polyomavirus. MCPyV infection is common, and seroprevalence studies indicate that widespread exposure begins early in life. The majority of adults have anti-MCPyV antibodies and there is a growing body of evidence that healthy human skin harbors resident or transient MCPyV suggesting that MCPyV infection persists throughout life. However, the mode of transmission, the host cells, and the latency characteristics of this virus remain to be elucidated. In addition, it is still not clear whether MCPyV is associated with diseases or lesions other than Merkel cell carcinoma. The etiologic role of MCPyV in MCC opens up opportunities to improve the understanding of this cancer and to potentially improve its treatment.

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“…MCPyV has been associated with cellular transformation in highly aggressive primary cutaneous neuroendocrine skin neoplasm, termed MCC, and is considered the only human PyV to date to cause tumors in its natural host (Arora et al 2012;Spurgeon and Lambert 2013). During detection of the virus, the LTAg was found to be truncated before the helicase domain in 80% of the cases (Duncavage et al 2009) but maintained the ability to bind retinoblastoma protein (Neumann et al 2011).…”

Section: Mcpyvmentioning

confidence: 99%

Entry, infection, replication, and egress of human polyomaviruses: an update

Bhattacharjee

Chattaraj

2017

Can. J. Microbiol.

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Polyomaviruses (PyVs), belonging to the family Polyomaviridae, are a group of small, nonenveloped, double-stranded, circular DNA viruses widely distributed in the vertebrates. PyVs cause no apparent disease in adult laboratory mice but cause a wide variety of tumors when artificially inoculated into neonates or semipermissive animals. A few human PyVs, such as BK, JC, and Merkel cell PyVs, have been unequivocally linked to pathogenesis under conditions of immunosuppression. Infection is thought to occur early in life and persists for the lifespan of the host. Over evolutionary time scales, it appears that PyVs have slowly co-evolved with specific host animal lineages. Host cell surface glycoproteins and glycolipids seem to play a decisive role in the entry stage of viral infection and in channeling the virions to specific intracellular membrane-bound compartments and ultimately to the nucleus, where the genomes are replicated and packaged for release. Therefore the transport of the infecting virion or viral genome to this site of multiplication is an essential process in productive viral infection as well as in latent infection and transformation. This review summarizes the major findings related to the characterization of the nature of the interactions between PyV and host protein and their impact in host cell invasion.

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MCV and Merkel cell carcinoma: a molecular success story

Cited by 95 publications

References 98 publications

The T Antigen Locus of Merkel Cell Polyomavirus Downregulates Human Toll-Like Receptor 9 Expression

The T Antigen Locus of Merkel Cell Polyomavirus Downregulates Human Toll-Like Receptor 9 Expression

Human Merkel cell polyomavirus: virological background and clinical implications

Entry, infection, replication, and egress of human polyomaviruses: an update

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