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Merkel Cell Polyomavirus Infection and Detection
Published on: February 7, 2019
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Merkel cell polyomavirus and Langerhans cell neoplasm
Ichiro Murakami1,2, Noriko Wada3, Junko Nakashima4,3
1Department of Pathology, Kochi Medical School, Kochi University, Kohasu, Okoh, Nankoku, Kochi, 783-8505, Japan. ichiro.murakami.09@gmail.com.
Cell Communication and Signaling : CCS
|August 24, 2018
Summary
Merkel cell polyomavirus (MCPyV) may cause Langerhans cell sarcoma (LCS) and Langerhans cell histiocytosis (LCH). MCPyV infection may trigger an IL-1 activation loop, proposing a new triple-factor model for LCH pathogenesis.
Area of Science:
- Oncology
- Virology
- Immunology
Background:
- Human sensitivity to external agents like viruses varies with individual health.
- Merkel cell polyomavirus (MCPyV), a skin-resident virus, has variable pathogenetic potential.
- MCPyV and Epstein-Barr virus are implicated in neoplastic and inflammatory diseases.
Purpose of the Study:
- To investigate the role of MCPyV in Langerhans cell sarcoma (LCS) and Langerhans cell histiocytosis (LCH).
- To explore potential pathogenetic mechanisms linking MCPyV to these conditions.
Main Methods:
- Meta-analysis of previous studies including quantitative PCR for MCPyV-DNA, proteomics, and immunohistochemistry.
- Construction of IL-17 endocrine and interleukin-1 (IL-1) activation loop models.
- Integration of data from multiple research groups.
Main Results:
- Subgroups associated with MCPyV as a causal agent were identified in LCS and LCH.
- LCS is a neoplastic lesion without inflammatory granuloma, distinct from LCH.
- MCPyV may be involved in the development of LCH, a proliferative disease with RAS/MAPK pathway mutations.
Conclusions:
- A subgroup of LCS may develop via mechanisms similar to Merkel cell carcinoma.
- LCH may arise from an inflammatory process sustained by gene mutations.
- MCPyV infection potentially triggers an IL-1 activation loop in LCH pathogenesis, suggesting a new triple-factor model.
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