摘要:
Merkel cell polyomavirus (MCV) was discovered in 2008 by molecular-based approaches in a rare neuroendocrine skin cancer, Merkel cell carcinoma (MCC). This new human member of the Polyomaviridae family of viruses raised considerable interest because studies of mammalian Polyomaviridae provided a significant part of our present knowledge on the molecular mechanisms of normal and cancer cell biology since the last 60 years. The role of MCV in oncogenesis is supported by evidence of monoclonal integration of MCV genome into host cells and/or mutations which abolish the ability of the virus to replicate and cause cell lysis, while they preserve its ability to interact with well-identified cellular tumour suppressors, thereby inducing cell proliferation. MCV appears to be a commensal of normal skin, where viral loads are the highest, and has also been detected at diverse body sites. While the precise life cycle of the virus in the host remains unknown, the cascade of steps that may lead to MCC has been deduced from experimental and clinical studies and includes impaired immunity, followed by accidental events provoking MCV integration and mutations, possibly favoured by as yet undefined cellular and/or environmental factors.
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