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The **human papillomavirus (HPV) E1-E2 protein-protein interface** is the physical interaction site between the viral E1 and E2 proteins, which cooperate to bind the viral origin of replication (ori), forming the E1-E2-ori complex that is essential for initiating viral DNA replication[1][2][5]. E1 is a viral helicase with DNA-binding and enzymatic (ATPase) activity, while E2 serves primarily as a transcriptional regulator and helps to recruit E1 to the viral origin, enhancing the specificity and efficiency of DNA binding and replication initiation[1][4][5]. Disruption of this protein-protein interface blocks the assembly of the replication complex, thereby inhibiting viral DNA replication, and has been investigated as a potential antiviral approach, especially in the context of diseases linked to persistent HPV infection such as cervical and other anogenital cancers[1][2].
Inhibition of protein-protein interface formation blocks initiation of papillomavirus DNA replication
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