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Updated: Oct 26, 2025

Merkel Cell Polyomavirus Infection and Detection
Published on: February 7, 2019
Merkel cell polyomavirus is a passenger virus in both poroma and porocarcinoma
Anna-Stiina Meriläinen1, Harri Sihto2, Virve Koljonen3
1Department of Surgery, The Central Hospital of Tavastia Proper, Hämeenlinna, Finland.
Background:
Merkel cell polyomavirus (MCPyV) has been studied in several malignant and nonmalignant tissues. However, only in Merkel cell carcinoma (MCC) has the connection to tumorigenesis been established. Previously, eccrine porocarcinoma samples were shown to express MCPyV in the majority of samples. We aimed to examine MCPyV in porocarcinoma and poroma samples using MCC as the reference material.
Methods:
We analyzed 17 porocarcinoma and 50 poroma samples for the presence of MCPyV using LT antigen immunostaining and DNA detection methods. In addition, 180 MCC samples served as controls.
Results:
MCPyV LT antigen immunostaining was detected in 10% of poroma and 18% of porocarcinoma samples; on the other hand, it was present in 65% of MCC samples. MCPyV DNA was detected in only 10% of poroma and porocarcinoma samples compared with 96% of MCC samples. The viral DNA copy number in all MCPyV DNA-positive MCCs was at least 25 times higher than that in porocarcinoma or poroma samples with the highest MCPyV DNA-to-PTPRG ratio.
Conclusions:
The low number of viral DNA copies in poroma and porocarcinoma samples, together with the negative LT expression of MCPyV DNA-positive tumors, indicates that MCPyV is simply a passenger virus rather than an oncogenic driver of porocarcinoma.
Insights
Merkel cell polyomavirus (MCPyV) is not an oncogenic driver in porocarcinoma. While found in some samples, low viral DNA and absent LT expression suggest MCPyV acts as a passenger virus, unlike in Merkel cell carcinoma.
Area of Science:
- Oncology
- Virology
- Dermatopathology
Background:
- Merkel cell polyomavirus (MCPyV) is linked to Merkel cell carcinoma (MCC) tumorigenesis.
- Previous studies indicated MCPyV expression in eccrine porocarcinoma.
- The role of MCPyV in poroma and porocarcinoma remains unclear.
Purpose of the Study:
- To investigate the presence and oncogenic potential of MCPyV in porocarcinoma and poroma.
- To compare MCPyV findings in porocarcinoma/poroma with MCC as a reference.
Main Methods:
- Analysis of 17 porocarcinoma and 50 poroma samples.
- MCPyV detection using LT antigen immunostaining and DNA analysis.
- Comparison with 180 MCC samples as controls.
Main Results:
- MCPyV LT antigen detected in 18% of porocarcinoma and 10% of poroma samples (vs. 65% in MCC).
- MCPyV DNA found in 10% of porocarcinoma/poroma (vs. 96% in MCC).
- Viral DNA copy numbers were significantly lower in porocarcinoma/poroma than in MCC.
Conclusions:
- MCPyV is unlikely to be an oncogenic driver in porocarcinoma.
- Low viral DNA load and lack of LT expression suggest MCPyV is a passenger virus in these tumors.
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