Merkel Cell Polyomavirus (MCPyV) and Cancers: Emergency Bell or False Alarm?

Abstract

Merkel cell polyomavirus (MCPyV), the sole member of Polyomavirus associated with oncogenesis in humans, is the major causative factor of Merkel cell carcinoma (MCC), a rare, neuroendocrine neoplasia of the skin. Many aspects of MCPyV biology and oncogenic mechanisms remain poorly understood. However, it has been established that oncogenic transformation is the outcome of the integration of the viral genome into the host DNA. The high prevalence of MCPyV in the population, along with the detection of the virus in various human tissue samples and the strong association of MCPyV with the emergence of MCC, have prompted researchers to further investigate the role of MCPyV in malignancies other than MCC. MCPyV DNA has been detected in several different non-MCC tumour tissues but with significantly lower prevalence, viral load and protein expression. Moreover, the two hallmarks of MCPyV MCC have rarely been investigated and the studies have produced generally inconsistent results. Therefore, the outcomes of the studies are inadequate and unable to clearly demonstrate a direct correlation between cellular transformation and MCPyV. This review aims to present a comprehensive recapitulation of the available literature regarding the association of MCPyV with oncogenesis (MCC and non-MCC tumours).

Role of the Microbiota in Skin Neoplasms: New Therapeutic Horizons

“…Furthermore, MCPyV has also been detected in other neoplasms affecting the oral cavity and the gastrointestinal system, in lung, renal, prostate, and cervical cancer, as well as in skin samples collected from healthy individuals [123]. Regarding soft tissue neoplasms, some studies have reported the presence of MCPyV in different NMSCs, the majority represented by SCCs affecting immunosuppressed patients, but also in AK, atypical fibroxantoma, keratoacanthoma, Kaposi's sarcoma, porocarcinoma, and dermatofibrosarcoma, despite the relatively low viral load and the lack of viral integration into the host genome having raised the question as to its possible coincidental rather than causal role in the genesis of such cancers [124][125][126].…”