Institute of Life Sciences, Chongqing Medical University, Chongqing, China.
Department of Otorhinolaryngology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
J Med Virol. 2024 Aug;96(8):e29815. doi: 10.1002/jmv.29815.
Human papillomaviruses (HPVs) are non-enveloped double-stranded DNA viruses. When HPV infection persists, infected tissues can develop many HPV-related diseases such as cervical cancer and head and neck squamous cell carcinoma. To establish their persistent infection, HPVs have evolved mechanisms to manipulate the host cellular processes such as DNA damage response (DDR), which includes homologous recombination, nonhomologous end joining, and microhomology-mediated end joining. Additionally, HPVs utilize host inflammatory processes to facilitate their life cycles. Here, we bridge the concepts of DDR and inflammatory response, and discuss how HPV proteins orchestrate a sophisticated manipulation of DDR and inflammation to promote their viral replication, ultimately fostering the progression of infected cells towards oncogenic transformation to malignancy.
人乳头瘤病毒（HPV）是无包膜的双链 DNA 病毒。当 HPV 感染持续存在时，受感染的组织可能会发展出多种与 HPV 相关的疾病，如宫颈癌和头颈部鳞状细胞癌。为了建立持续感染，HPV 进化出了操纵宿主细胞过程的机制，如 DNA 损伤反应（DDR），其中包括同源重组、非同源末端连接和微同源介导的末端连接。此外，HPV 还利用宿主的炎症过程来促进其生命周期。在这里，我们将 DDR 和炎症反应的概念联系起来，并讨论 HPV 蛋白如何巧妙地操纵 DDR 和炎症，以促进其病毒复制，最终促使受感染的细胞向致癌转化为恶性。
