Human papillomaviruses (HPVs) are small, non-enveloped viruses with circular double-stranded DNA. Over 400 HPV types have been identified, with more than 180–220 fully classified. HPV infections are among the most common pathogens, causing 5% of all cancers globally, including cervical, anal, vaginal, penile, and head and neck cancers. While most infections are asymptomatic, persistent or recurrent benign lesions such as warts are common. HPV is resistant to many disinfectants and external conditions, and no drug exists to inhibit viral replication. Treatment typically involves lesion removal or immune stimulation. This review discusses the classification, structure, and pathogenesis of HPV, focusing on the roles of E6, E7, and other viral proteins in benign and cancerous lesions. It also explores new therapeutic approaches, including substances that block HPV entry, inhibitors of viral proteins, and plant-derived compounds. The paper highlights the importance of HPV classification, with HPV types divided into alphapapillomaviruses and betapapillomaviruses. The HPV genome is divided into E (early), L (late), and LCR (long control region) regions, with E6 and E7 playing key roles in oncogenesis. HPV replication begins with viral entry through epithelial wounds, followed by DNA release and replication in the basal layer. The E1 and E2 proteins are crucial for viral DNA replication, while E6 and E7 inhibit apoptosis and promote cell proliferation. Persistent infections can lead to integration of viral DNA into host DNA, contributing to cancer development. However, not all HPV infections result in cancer, and integration is not always required for carcinogenesis. Immune responses to HPV are primarily mediated by cell-mediated immunity, with CD8+ and CD4+ T cells targeting E6, E7, and E2 proteins. Prophylactic vaccines, such as Gardasil and Cervarix, induce high antibody titers and are effective in preventing HPV infections. Therapeutic vaccines, which target E6 and E7, are being developed to treat HPV-related lesions and cancers. Current treatments include surgical methods and topical agents like 5-fluorouracil, cantharidin, and podophyllotoxin, which inhibit viral replication and cell proliferation. New therapeutic strategies, including vaccines based on L2 proteins and RNA vaccines, are under investigation. The review emphasizes the need for further research into HPV pathogenesis and novel therapeutic approaches to improve treatment outcomes.Human papillomaviruses (HPVs) are small, non-enveloped viruses with circular double-stranded DNA. Over 400 HPV types have been identified, with more than 180–220 fully classified. HPV infections are among the most common pathogens, causing 5% of all cancers globally, including cervical, anal, vaginal, penile, and head and neck cancers. While most infections are asymptomatic, persistent or recurrent benign lesions such as warts are common. HPV is resistant to many disinfectants and external conditions, and no drug exists to inhibit viral replication. Treatment typically involves lesion removal or immune stimulation. This review discusses the classification, structure, and pathogenesis of HPV, focusing on the roles of E6, E7, and other viral proteins in benign and cancerous lesions. It also explores new therapeutic approaches, including substances that block HPV entry, inhibitors of viral proteins, and plant-derived compounds. The paper highlights the importance of HPV classification, with HPV types divided into alphapapillomaviruses and betapapillomaviruses. The HPV genome is divided into E (early), L (late), and LCR (long control region) regions, with E6 and E7 playing key roles in oncogenesis. HPV replication begins with viral entry through epithelial wounds, followed by DNA release and replication in the basal layer. The E1 and E2 proteins are crucial for viral DNA replication, while E6 and E7 inhibit apoptosis and promote cell proliferation. Persistent infections can lead to integration of viral DNA into host DNA, contributing to cancer development. However, not all HPV infections result in cancer, and integration is not always required for carcinogenesis. Immune responses to HPV are primarily mediated by cell-mediated immunity, with CD8+ and CD4+ T cells targeting E6, E7, and E2 proteins. Prophylactic vaccines, such as Gardasil and Cervarix, induce high antibody titers and are effective in preventing HPV infections. Therapeutic vaccines, which target E6 and E7, are being developed to treat HPV-related lesions and cancers. Current treatments include surgical methods and topical agents like 5-fluorouracil, cantharidin, and podophyllotoxin, which inhibit viral replication and cell proliferation. New therapeutic strategies, including vaccines based on L2 proteins and RNA vaccines, are under investigation. The review emphasizes the need for further research into HPV pathogenesis and novel therapeutic approaches to improve treatment outcomes.