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Human papillomavirus-infected keratinocytes are epithelial cells of the skin or mucosa that have been infected by human papillomavirus (HPV). These cells serve as the primary site for productive HPV infection. The virus manipulates cellular pathways—most notably through its E6 and E7 oncoproteins—to disrupt normal cell cycle control, inhibit apoptosis, and evade immune detection. This allows continued proliferation of infected cells and supports completion of the viral life cycle. Persistent infection with high-risk HPV types can lead to deregulated gene expression in these cells, resulting in neoplastic progression and cancer development—especially cervical cancer but also certain skin cancers in immunocompromised individuals. While these cells are central to disease pathogenesis, they are not themselves considered canonical therapeutic targets like receptors or enzymes; instead, therapies focus on preventing infection (e.g., vaccination), eliminating virally transformed cells via immune mechanisms, or targeting specific viral proteins within these host cells[1][2][3][4][5].
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