Lymphotropism of MCPyV, Nova Scotia, Canada | CDC EID

EID Journal Home > Volume 16, Number 11–November 2010
Volume 16, Number 11–November 2010
Research
Lymphotropism of Merkel Cell Polyomavirus Infection, Nova Scotia, Canada

Sonia Toracchio, Annette Foyle, Vojtech Sroller,1 Jon A. Reed, Jun Wu, Claudia A. Kozinetz, and Janet S. Butel Comments to Author
Author affiliations: Baylor College of Medicine, Houston, Texas, USA (S. Toracchio, V. Sroller, J.A. Reed, C.A. Kozinez, J.S. Butel); Dalhousie University, Halifax, Nova Scotia, Canada (A. Foyle); Queen Elizabeth II Health Science Center, Halifax (A. Foyle); and Public Health Agency of Canada, Ottawa, Ontario, Canada (J. Wu)

Suggested citation for this article

Abstract
To test the hypothesis that Merkel cell polyomavirus (MCPyV) can infect cells of the lymphoid system, we analyzed 353 specimens, including 152 non-Hodgkin lymphomas, 44 Hodgkin lymphomas, 110 benign lymph nodes, 27 lymph nodes with metastasis, and 20 extranodal tissue samples. MCPyV DNA was detected by quantitative PCR in 13 (6.6%) of 196 lymphomas, including 5 (20.8%) of 24 chronic lymphocytic leukemia specimens, and in 11 (10%) of 110 benign lymph nodes, including 8 (13.1%) of 61 samples of reactive hyperplasia and 3 (10.3%) of 29 normal lymph nodes. Other samples were MCPyV negative. Sequence analysis of 9 virus-positive samples confirmed the identity of MCPyV; 3 viral strains were represented. Immunohistochemical testing showed that 1 T-cell lymphoma expressed MCPyV T-antigen. These findings suggest that the lymphoid system plays a role in MCPyV infection and may be a site for MCPyV persistence.

Merkel cell polyomavirus (MCPyV) was first described in 2008 (1) as a new human virus associated with Merkel cell carcinoma (MCC), an uncommon but aggressive form of skin cancer. Subsequent studies have reported the presence of MCPyV in 24%–100% of MCCs from patients from the United States, Germany, France, the Netherlands, and Australia (1–11). Findings of the clonal integration of MCPyV in tumor cell genomes, tumor-associated mutations in the large T-antigen (T-ag) gene, and large T-ag expression in tumors suggest that MCPyV is not only associated with MCC, but that it may be the causative agent (1,12,13). However, the natural reservoir of MCPyV in infected hosts remains to be identified. MCPyV DNA has been detected at low copy number in some non-MCC skin tumors, in normal tissues of skin and the gastrointestinal tract, and in a few nasopharyngeal aspirates and blood samples, including inflammatory monocytes (1,5,6,11,14–16).

Lymphocytes can disseminate viruses throughout a host and may provide sites of viral persistence. Human polyomaviruses are known to establish persistent infections in healthy persons, to undergo periodic reactivation and replication, and to cause disease in susceptible hosts. Some polyomaviruses are lymphotropic; BK virus, simian virus 40, and JC virus DNA sequences have been detected in human lymphoid tissues, blood cells, and lymphomas (17–20). Recently, Shuda et al. (13) reported the presence of MCPyV in a low percentage (2.2%) of hematolymphoid malignancies. In this study, we investigated the presence of MCPyV in benign lymph nodes and malignant lymphomas in patients from Canada.

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Lymphotropism of MCPyV, Nova Scotia, Canada | CDC EID


Suggested Citation for this Article

Toracchio S, Foyle A, Sroller V, Reed JA, Wu J, Kozinetz CA, et al. Lymphotropism of Merkel cell polyomavirus infection, Nova Scotia, Canada. Emerg Infect Dis [serial on the Internet]. 2010 Nov [date cited]. http://www.cdc.gov/EID/content/16/11/1702.htm

DOI: 10.3201/eid1611.100628

1Current affiliation: Institute of Hematology and Blood Transfusion, Prague, Czech Republic