Human papillomavirus type 16 and 18 virions (HPV-16/18)

Human papillomavirus (HPV) types 16 and 18 are high-risk, non-enveloped DNA viruses that serve as the primary causative agents for approximately 70% of cervical cancers and a significant proportion of other anogenital and oropharyngeal malignancies [2, 14, 21]. The virion structure consists of a circular double-stranded DNA genome protected by an icosahedral capsid composed of the major structural protein L1 and the minor protein L2 [8, 23]. These viruses infect the basal cells of the epithelium, utilizing the L1 protein to bind host cell receptors and initiate endocytosis [22, 23]. Prophylactic vaccines, including Gardasil and Cervarix, target the L1 protein to elicit neutralizing antibodies that prevent initial infection [6, 14, 19]. In persistent infections, the viral genome often integrates into the host DNA, leading to the over-expression of E6 and E7 oncoproteins, which degrade the tumor suppressors p53 and pRb, respectively, to drive malignant transformation [1, 5, 18]. Consequently, while current vaccines are highly effective at prevention, therapeutic strategies targeting these oncoproteins are under active development to treat existing HPV-associated lesions and cancers [6, 9, 14].

Other names

HPV16HPV18Human papillomavirus 16Human papillomavirus 18High-risk HPV 16/18HPV-16/18 virions

Prophylactic vaccines induce neutralizing antibodies against the L1 capsid protein to block viral attachment and entry into host cells; therapeutic candidates target E6/E7 oncoproteins to induce T-cell mediated destruction of infected cells.