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Human papillomavirus type 57 (HPV-57) is a double-stranded DNA virus belonging to the Alphapapillomavirus genus of the Papillomaviridae family (UniProt [3]). It is primarily associated with the development of common warts (verrucae vulgares) and oral papillomas, but it has also been identified in more serious lesions, including inverted papillomas of the nasal cavity and periungual squamous cell carcinomas (PubMed [7, 12]). Unlike the well-known high-risk mucosal types like HPV-16 and HPV-18, HPV-57 is often categorized as a cutaneous type, yet it possesses significant oncogenic potential through its E6 and E7 oncoproteins (PubMed [7]). These viral proteins facilitate cellular transformation by inducing the degradation of the tumor suppressor p53 and inactivating the retinoblastoma protein (pRb), respectively, thereby deregulating the cell cycle and promoting immortalization (PMC [1, 4, 6]). There are currently no drugs specifically approved to target HPV-57; however, various non-specific therapeutic modalities are employed to manage its clinical manifestations (Medscape [19]). These include topical immunomodulators like imiquimod, which stimulates the innate immune response via TLR7, and cytotoxic agents such as podofilox and 5-fluorouracil that inhibit viral-induced cell proliferation (PMC [18], Medscape [19]). Experimental treatments and case reports have also explored the use of the antiviral cidofovir and the Src kinase inhibitor tirbanibulin (PMC [12, 18]). Notably, HPV-57 is not covered by current 9-valent prophylactic vaccines, presenting a challenge for prevention in populations at risk for its associated cutaneous and mucosal malignancies (PMC [10, 13]).
Toll-like receptor 7 agonist, Antimetabolite, DNA polymerase inhibitor, Tubulin polymerization inhibitor, Src kinase inhibitor, Mitotic inhibitor
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