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Published on: October 25, 2018
Human Parvovirus B19 May Be a Risk Factor in Myasthenia Gravis with Thymoma
Li Gong1, Jing Tian1, Yan Zhang1
1Department of Pathology, Helmholtz Sina-German Research Laboratory for Cancer, Tangdu Hospital, Air Force Medical University, Xi'an, People's Republic of China.
Human parvovirus B19 (B19V) infection is linked to ectopic germinal centers (GCs) in thymomas. This finding suggests B19V plays a key role in the development of thymoma-associated myasthenia gravis (MG).
Area of Science:
- Immunology
- Virology
- Pathology
Background:
- Myasthenia gravis (MG) pathogenesis is complex, with thymic abnormalities implicated.
- Human parvovirus B19 (B19V) has been previously associated with thymic hyperplasia-related MG.
- Further investigation is needed to clarify the role of B19V in thymoma-associated MG.
Purpose of the Study:
- To investigate the relationship between B19V and thymoma-associated myasthenia gravis (MG).
- To assess the prevalence of B19V DNA and VP2 protein in thymomas.
- To correlate B19V presence with clinicopathological features, including germinal centers (GCs) and MG.
Main Methods:
- Analysis of 708 thymoma cases.
- Detection of B19V DNA using nested and quantitative PCR.
- Immunohistochemistry and fluorescent multiplex immunohistochemistry for B19V VP2 protein.
- Electron microscopy for viral particle visualization.
- Correlation with clinicopathological data, including MG and GCs.
Main Results:
- Patients with MG or ectopic GCs were significantly younger.
- Ectopic GCs were more frequent in thymomas associated with MG.
- B19V DNA positivity correlated significantly with the presence of GCs.
- B19V VP2 protein was detected in neoplastic thymic epithelial cells and GCs.
- B19V particles were observed in TECs and B cells within GCs.
Conclusions:
- The pathogenesis of MG is strongly linked to the presence of ectopic GCs in thymomas.
- B19V infection is a plausible contributor to the formation of ectopic GCs in thymoma.
- This study provides novel insights into the etiopathogenic mechanisms of B19V in thymoma-associated MG.
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