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J Am Acad Dermatol. 2012 Jul;67(1):41-6. doi: 10.1016/j.jaad.2011.07.026. Epub 2011 Oct 11.

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

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  • 1Institute of Virology, National Reference Centre for Papilloma- and Polyomaviruses, University of Cologne, Cologne, Germany.



Merkel 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).


To 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.


Paraffin-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.


A 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.


The relatively small number of samples is a limitation.


Our findings argue against a pathogenic role of MCPyV in KA and SCC.

Copyright © 2011 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.

[PubMed - indexed for MEDLINE]
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