Human papillomavirus (HPV) infection is a necessary cause of cervical neoplasia. Concomitant infection with other infectious agents has been demonstrated to be a cofactor for HPV-related cervical carcinogenesis. The present investigation aimed to determine the prevalence of HPV and Merkel cell polyomavirus (MCPyV) infections and to evaluate the role of MCPyV as a co-factor for HPV-related cervical carcinogenesis in Iranian women. From 2011 to 2013, a total of 112 cervical samples were examined. Forty-five samples (40.2 %) were positive for HPV. MCPyV was found in 37 samples (33 %). Both HPV and MCPyV were present in 14 samples (12.5 %). MCPyV was seen in 30 % of squamous cell carcinomas, 37.5 % of adenocarcinomas, and 16.7 % of undifferentiated carcinomas. The MCPyV large T antigen (LT-Ag) DNA load was determined as the viral copy number per cell. The median MCPyV LT-Ag copy number in positive women was 0.049 × 10 −3 per cell (range 0.0006 × 10 −3 -4.558 × 10 −3 copies per cell). In comparison with other types of cervical cancer, the MCPyV LT-Ag load was higher in adenocarcinomas (0.1024 × 10 −3 copies per cell). A logistic regression model adjusted to HPV positivity and age revealed no statistically significant association between MCPyV infection and cervical cancer (OR, 1.12; 95 % CI, 0.07-16.83). More studies should be conducted to clarify the role of MCPyV in cervical carcinogenesis.
Archives of Virology – Springer Journals
Published: May 1, 2015
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