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Human papillomavirus type 16 (HPV16) is a high-risk, non-enveloped double-stranded DNA virus belonging to the Papillomaviridae family [1]. The virion is composed of a 7.9 kb circular genome encased in an icosahedral capsid consisting of major (L1) and minor (L2) proteins [2]. HPV16 is the primary etiological agent for approximately 50% of cervical cancers and a significant proportion of other anogenital and oropharyngeal malignancies [3]. Its oncogenic potential is largely driven by the expression of E6 and E7 oncoproteins, which degrade host tumor suppressors p53 and pRb, respectively [4]. Current therapeutic strategies primarily focus on prevention through vaccines that target the L1 capsid protein to elicit neutralizing antibodies [5]. Research into therapeutic vaccines and small molecule inhibitors continues to target the viral life cycle and oncogenic proteins to treat existing infections and HPV-associated lesions [6].
Preventative vaccines utilize recombinant L1 capsid proteins to form virus-like particles (VLPs) that induce high titers of neutralizing antibodies, preventing viral entry into host basal epithelial cells [5, 7]. Therapeutic approaches under investigation target the E6 and E7 oncoproteins to induce cellular immune responses, specifically CD8+ T-cell activation, to eliminate infected or transformed cells [8].
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