HPV

HPV is a small, non-enveloped dsDNA virus in the Papillomaviridae family that infects squamous epithelium of the skin and mucosa. It is transmitted primarily via sexual contact (also skin-to-skin) and is the most prevalent STI worldwide. Over 150 subtypes exist, categorized by oncogenic potential.

Low-risk types (especially 6 and 11) cause benign lesions such as condylomata acuminata (genital warts) and laryngeal papillomatosis, typically producing koilocytic changes on histology without malignant transformation.

High-risk types (especially 16 and 18, also 31, 33, 45) are oncogenic and account for the majority of cervical cancers, as well as significant proportions of anal, vulvar, vaginal, penile, and oropharyngeal squamous cell carcinomas. Oncogenesis occurs through viral proteins E6 and E7: E6 promotes degradation of p53 (tumor suppressor), while E7 inactivates retinoblastoma protein (Rb), leading to unchecked cell cycle progression and loss of apoptotic control. Persistent infection with high-risk HPV, particularly in the cervical transformation zone, can progress through cervical intraepithelial neoplasia (CIN I-III) to invasive carcinoma.

Clinical detection includes Pap smear cytology (to detect dysplastic changes) and HPV DNA co-testing in cervical cancer screening. Colposcopy with biopsy is used for further evaluation of abnormal results. Histologic hallmark of HPV infection is the koilocyte—a squamous cell with a perinuclear halo and nuclear atypia.

Prevention centers on the HPV vaccine (e.g., Gardasil 9), which targets multiple high- and low-risk strains and is recommended for adolescents of all genders before sexual debut. Vaccination has significantly reduced rates of cervical dysplasia and genital warts in vaccinated populations.

Board relevance: Know the E6/p53 and E7/Rb mechanism, association of HPV 16/18 with cervical/anal/oropharyngeal cancer, HPV 6/11 with genital warts and laryngeal papillomatosis, koilocyte histology, and the role of Pap smear/HPV co-testing in screening.