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Human Papillomavirus (HPV) types 6, 11, 16, and 18 are double-stranded DNA viruses belonging to the Papillomaviridae family that specifically infect human epithelial cells [1]. Types 16 and 18 are high-risk oncogenic strains responsible for approximately 70% of cervical cancer cases worldwide, as well as a significant proportion of anal, vulvar, vaginal, and oropharyngeal cancers [2]. In contrast, types 6 and 11 are low-risk strains that cause approximately 90% of genital warts (condyloma acuminata) and recurrent respiratory papillomatosis [3]. The primary therapeutic approach involves the use of virus-like particles (VLPs) composed of the L1 major capsid protein to induce a protective immune response [4]. These vaccines, such as the quadrivalent and nonavalent formulations, stimulate the production of neutralizing antibodies that prevent the virions from binding to and entering host cells [5]. While highly effective as a prophylactic measure, these interventions do not eliminate pre-existing viral DNA or treat established HPV-related lesions [6].
Induction of a robust humoral immune response and production of neutralizing antibodies against the L1 major capsid protein to prevent viral attachment and entry into host cells.
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