Abstract
Viruses are the cause of approximately 15% of all human cancers. Both RNA and DNA human tumor viruses have been identified, with Merkel cell polyomavirus being the most recent one to be linked to cancer. This virus is associated with about 80% of Merkel cell carcinomas, a rare, but aggressive cutaneous malignancy. Despite its name, the cells of origin of this tumor may not be Merkel cells. This review provides an update on the structure and life cycle, cell tropism and epidemiology of the virus and its oncogenic properties. Putative strategies to prevent viral infection or treat virus-positive Merkel cell carcinoma patients are discussed.
Highlights
Because MCPyVMerkel cell polyomavirus (MCPyV) was originally detected in MCC, a tumor believed to originate from Merkel cells (MCs), which are specialized skin cells, and is chronically shed from skin from healthy individuals, it was believed that the virus is dermatotrophic
MCPyV DNA has been detected in cutaneous swabs [45] and it is possible that infected dermal fibroblasts might die and virions could be carried to the skin surface by the flow of differentiating keratinocytes [46]
Dermal fibroblasts were suggested since they are permissive for MCPyV infection [44], and keratinocytes could be the cell of origin of VP-MCC because keratinocyte-specific expression of MCPyV oncoproteins resulted in oncogenic effects [76]
Summary
Merkel cell polyomavirus (MCPyV) is a naked double-stranded DNA virus belonging to the Polyomaviridae family [1]. Replication by reducing the binding affinity of LT to the viral origin of replication (ORI), while T299 truncation of the C-terminal region of LT and phosphorylation of specific residues in LT may phosphorylation affects both binding to and unwinding of the DNA [15]. At its unique C-terminal region, sT encompasses two zinc-binding domains (CXCXXC motif), which provide structural and functional stabilities and two domains rich in cysteine and proline residues responsible for the sT interaction with protein phosphatase 2A (PP2A) (see further) [17]. Interspersed between the early and late region is the non-coding control region (NCCR), which contains the ORI characterized by a core of 71-bp sufficient to initiate DNA replication (Figure 1) This core region consists of an AT rich tract and eight 50 -GAGGC-30 LT binding motifs [12]. This could explain how MCPyV may have been transmitted from apes to humans [32]
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