No evidence for a causal role of Merkel cell polyomavirus in keratoacanthoma

BackgroundMerkel cell polyomavirus (MCPyV) is a recently discovered virus that is monoclonally integrated into the genome of approximately 80% of all Merkel cell carcinomas (MCCs). While some evidence exists that MCPyV does not play a pathogenic role in other nonmelanoma skin cancers, such as basal cell carcinoma and squamous cell carcinoma (SCC), little is known about the presence of MCPyV in keratoacanthoma (KA).ObjectivesTo evaluate the prevalence, viral DNA-load, and large T(umor)-antigen expression of MCPyV in KA of immunocompetent patients and to compare the results with those found in SCC and MCC.MethodsParaffin-embedded tissue samples were analyzed for the presence of MCPyV-DNA by polymerase chain reaction (PCR). MCPyV-DNA load (MCPyV-DNA copies per beta-globin gene copy) was determined by using quantitative real-time PCR. Immunohistochemical analysis of the MCPyV large T-antigen was performed with the monoclonal antibody CM2B4.ResultsA total of 137 samples (42 KA, 52 SCC, and 43 MCC) were analyzed. MCPyV-DNA was found significantly more frequently in MCC (37/43, 86.0%) compared with KA (12/42, 28.6%) and SCC (14/52, 26.9%). Moreover, MCPyV-DNA loads were more than two orders of magnitude lower in KA and SCC compared with MCC (median/mean loads 0.005/0.015 [KA] vs 0.023/0.059 [SCC] vs 2.613/56.840 [MCC] MCPyV-DNA copies per beta-globin gene copy). All MCC analyzed (n = 3) expressed MCPyV large T-antigen, whereas 8 KA and 7 SCC were negative in immunohistochemistry.LimitationsThe relatively small number of samples is a limitation.ConclusionsOur findings argue against a pathogenic role of MCPyV in KA and SCC.