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Human papillomavirus type 45 (HPV-45) is a high-risk, non-enveloped, double-stranded DNA virus belonging to the Alphapapillomavirus 7 species, making it phylogenetically similar to HPV-18 (IARC, 2012). It is a major causative agent of invasive cervical cancer, often identified as the third or fourth most common HPV type in malignant lesions worldwide (Sancho-Garnier et al., 2013). The virion structure consists of an icosahedral capsid formed by the major L1 and minor L2 proteins, which are essential for binding to the basement membrane and entering basal epithelial cells (Buck et al., 2013). Once the virus establishes infection, it expresses the E6 and E7 oncoproteins, which facilitate oncogenesis by promoting the degradation of host tumor suppressor proteins p53 and pRb, respectively (Moody & Laimins, 2010). Therapeutic intervention is primarily prophylactic, utilizing the 9-valent HPV vaccine (Gardasil 9) to elicit neutralizing antibodies against the L1 protein, thereby blocking viral entry (FDA, 2014). While highly effective at preventing infection, HPV-45 remains a significant clinical challenge due to its ability to integrate into the host genome and persist in a latent state (Doorbar et al., 2012).
Active immunization via the production of neutralizing antibodies against the L1 protein, preventing viral attachment and entry into host cells.
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