Prevalence of Merkel Cell Polyomavirus (MCPyV) in the Oral Cavity Biopsies in Northern Iran

Abstract

Objective: Infection with human tumor viruses is one of the hypothesized causes of cancer. The current investigation aimed to explore the presence and quantitative analysis of a new human tumor virus, Merkel cell polyomavirus (MCPyV) in tissue samples of 114 patients with oral cavity lesions including oral squamous cell carcinoma (OSCC), oral lichen planus (OLP), Dysplasia and oral irritation fibroma (OIF) in Northern Iran. Methods: From 114 formalin fixed paraffin embedded samples; 35 with SCC, 29 with OLP, 14 with dysplasia and 36 with OIF were cut, deparaffinized and DNA was extracted. Quantitative detection of MCPyV large T antigen was performed by absolute quantitative Real-Time PCR. Result: MCPyV DNA was detected in 30.6% (n: 11/36) of IF, 24.1% (n; 7/29) of OLP, 21.4% (n:3/14) of dysplasia and 20% (n;7/35) of OSCC samples. The mean MCPyV DNA copy number was 2.32×10 −2 ± 3.97 ×10 −2 , 2.02×10 −2 (SD=3.13×10 −2 ), 2.69×10−4 (SD=2.51×10 −4 ), and 2.56×10 −4 (SD=6.73×10 −4 ) per cell in OSCC, dysplasia and both of OLP and OIF samples, respectively (P=0.76). Conclusion: This study provides the first data from Iran regarding the presence of MCPyV genome in oral cavity lesions and oral cancer. These results also emphasize that MCPyV has an active role in the occurrence of oral lesions and progression to cancer. Further studies should be carried out to clarify the role of MCPyV in oral cavity lesions.

Merkel Cell Polyomavirus in the Context of Oral Squamous Cell Carcinoma and Oral Potentially Malignant Disorders

“…To investigate whether this oncogenic virus could be involved in the etiology of oral cavity tumors, in the current study, MCPyV prevalence and the molecular state were examined. MCPyV DNA was detected in both neoplastic and non-neoplastic oral tissue, suggesting that MCPyV positivity is not correlated with cancerous or non-cancerous oral lesions, as previously reported [30,45,46]. Moreover, the difference between viral load in OSCC and OPMD was not statistically significant; indeed, both tumor and non-tumor samples reported a low copy number of MCPyV DNA, about 1.49 × 10 2 copies/mL, suggesting that the virus could establish a persistent replication in the oral cavity, without any pathological outcome [30].…”

“…Considering the oncogenic potentials of MCPyV and its widespread prevalence among the human population, several studies have been carried out to elucidate a plausible role of MCPyV in the development of non-MCC tumors. MCPyV has been identified in various other cancers, amongst them head and neck tumors (HN), including esophagus and oral cavities [7,[27][28][29][30][31][32]. However, in most cases the presence of viral DNA was examined, whereas expression of viral genes, state of the viral genome, and the possible truncation of LTAg was not investigated.…”

Immunological evidence of an early seroconversion to oncogenic Merkel cell polyomavirus in healthy children and young adults

“…Although MCPyV is oncogenic, its infection is asymptomatic and widespread in humans [17][18][19]. Soon after the primary infection, MCPyV elicits a physiological immune response, while being maintained in a latent/persistent state throughout life in immunocompetent hosts [20].…”