Molecular Inflammation Research Group, Department of Medical Biology, University of Tromsø - The Arctic University of Norway, Tromsø, Norway.
APMIS. 2020 Feb;128(2):104-120. doi: 10.1111/apm.13019. Epub 2020 Jan 28.
Merkel cell polyomavirus (MCPyV) is the major causative factor of the rare but aggressive cancer, Merkel cell carcinoma (MCC). Two characteristics of MCPyV-positive MCCs are integration of the viral genome and expression of a truncated version of one of its oncogenic proteins, namely large T antigen. The strong association of MCPyV with MCC development has incited researchers to further investigate a possible role of this virus in other cancers. However, many of the examples displaying the presence of the virus in the various non-MCC cancers are not able to clearly demonstrate a direct connection between cellular transformation and the presence of the virus. The prevalence of the virus is significantly lower in non-MCC cancers compared to MCCs, with a lower level of viral load and sparse viral protein expression. Moreover, the state of the viral genome, and whether a truncated large T antigen is expressed, has rarely been investigated. Nonetheless, considering the strong oncogenic potential of MCPyV proteins in MCC, the plausible contribution of MCPyV to transformation and cancer growth in non-MCC tumors cannot be ruled out. Furthermore, the absence of MCPyV in cancers does not exclude a hit-and-run mechanism, or the oncoproteins of MCPyV may potentiate the neoplastic process mediated by co-infecting oncoviruses such as high-risk human papillomaviruses and Epstein-Barr virus. The current review is focusing on the available data describing the presence of MCPyV in non-MCC tumors, with an aim to provide a comprehensive overview of the corresponding literature and to discuss the potential contribution of MCPyV to non-MCC cancer in light of this.
默克尔细胞多瘤病毒（Merkel cell polyomavirus，MCPyV）是罕见但侵袭性较强的默克尔细胞癌（Merkel cell carcinoma，MCC）的主要致病因素。MCPyV 阳性 MCC 的两个特征是病毒基因组的整合和其一种致癌蛋白——大 T 抗原的截断版本的表达。MCPyV 与 MCC 发展的强烈关联促使研究人员进一步研究该病毒在其他癌症中的可能作用。然而，许多显示病毒存在于各种非 MCC 癌症中的例子不能明确证明细胞转化与病毒存在之间的直接联系。与 MCC 相比，该病毒在非 MCC 癌症中的流行率明显较低，病毒载量较低，病毒蛋白表达稀疏。此外，病毒基因组的状态以及是否表达截断的大 T 抗原很少被研究。尽管如此，考虑到 MCPyV 蛋白在 MCC 中的强烈致癌潜力，MCPyV 对非 MCC 肿瘤的转化和癌症生长的可能贡献不能排除。此外，非 MCC 癌症中缺乏 MCPyV 并不能排除“打了就跑”机制，或者 MCPyV 的致癌蛋白可能增强共感染的致癌病毒（如高危型人乳头瘤病毒和 Epstein-Barr 病毒）介导的肿瘤发生过程。本综述重点关注描述非 MCC 肿瘤中存在 MCPyV 的现有数据，旨在提供相应文献的全面概述，并根据这些数据讨论 MCPyV 对非 MCC 癌症的潜在贡献。
