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Human polyomavirus-6 levels may contribute to epithelial proliferations in BRAF therapy

Among patients receiving therapy with BRAF inhibitors, recently published study data indicated the presence of higher human polyomavirus-6 DNA load and VP1 protein may contribute to the development of epithelial proliferations.

Researchers retrospectively analyzed 18 biopsy samples from six patients with melanoma who developed epithelial proliferations after beginning treatment with the BRAF inhibitor, vemurafenib, to determine the presence of the most frequently observed RAS mutations, the detection of viruses using real-time polymerase chain reaction and the presence of capsid proteins from the virus most frequently detected on immunohistochemical analysis.

Of the 16 samples with clear results, the researchers identified 10 RAS mutations. Although almost no DNA for human polyomavirus-9 (HPyV-9), HPyV-10 or trichodysplasia spinulosa-associated polyomavirus (TSPyV) was present among the samples, DNA of Merkel cell polyomavirus (MCPyV) was present in 13 of the 18 samples, and human papillomavirus (HPV), HPyV-6 and HPyV-7 DNA were found to be present in all of the samples, according to the researchers.

Several samples from one patient contained high amounts of HPyV-6 DNA as well as VP1 protein expression, suggesting a contribution of HPyV-6 to the pathogenesis of the inhibitor-induced epithelial proliferations. However, the researchers concluded that the relative impact appeared to be circumstantial compared with the relative impact of RAS mutations.

Disclosure: The authors have no relevant financial disclosures.