Utilizing capsid protein-specific antibodies and viral T-antigen oncoproteins to elicit active immunity against virus positive Merkel cell carcinoma

Abigail Meek


This microreview investigates the recent progress made towards a preventative or therapeutic vaccine against Merkel cell carcinomas’ (MCC) causative agent, Merkel cell polyomavirus’ (MCPyV). MCC is the malignant growth in the skin, usually caused by prolonged/repeated exposure to harmful UV rays or a compromised immune system in the host. It has been shown that when higher levels of antibodies that specifically target VP1 a capsid protein, the survival rate of this aggressive cancer is higher. The objective of clinical research is to upregulate anti-VP1 immune response via vaccination to slow or even stop MCC growth. Using both VP1-specific CD4+ and CD8+ T cells, it was found that antitumor efficacy was dose dependent, and slowed the progression of CMS5-VP1 tumors in trials using mice with MCV-related MCC. Alternative research has focused on utilizing anti-PD-(L)1 checkpoint inhibitors, as PD-(L)1 inhibits T cell function against pathogenic cells. It has been shown that combination therapies to boost immune response while upregulating T cell response have been successful. It has been suggested that combining these aforementioned therapies with viral T-Ag oncoproteins from genomically integrated MCPyV would be more beneficial than monotherapy. T-Ag is responsible for eliciting specific B and T cell responses, and is required to drive virus-positive MCC cell proliferation. This suggests that using T-Ag in a therapeutic vaccination against MCPyV has merit to, when in combination with other immunotherapies, increase survival rate.

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