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Research shows that HPV E6 and E7 proteins engage host factors to create an environment that favors viral replication while rewiring host signaling to promote proliferation, block differentiation, and reduce cell death. Because dysregulated “high-risk” E6/E7 expression is sufficient to sustain HPV-associated cancers, efforts aim to define which host targets are critical cancer drivers. 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Defining the cancer-driving targets helps clarify the distinct roles of other interactions and supports focusing anti-cancer therapy on the virus-host interfaces with the greatest therapeutic impact.","Answer","https://schema.org",{"og:url":83,"og:type":116,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":118,"canonical":83},"index,follow",{"doc_id":120,"site_id":62},337010,1790123709,{"code":4,"msg":5,"data":123},{"doc_id":120,"user_id":124,"nickname":92,"user_avatar":125,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":126,"file_id":127,"file_url":128,"file_type":129,"file_size":130,"view_count":39,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":131,"language":132,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":133,"faqs":134,"seo_title":135,"seo_description":67,"update_tm":136,"read_time":41},962075114765,"https://ap-avatar.wpscdn.com/davatar_a8503ba1806abce46bf441b54a3ca4cd","| Virology | Minireview  \nWhat are the essential determinants of human papillomavirus carcinogenesis?  \nKarl Munger,1 Elizabeth A. White2  \nAUTHOR AFFILIATIONS See affiliation list on p. 9.  \nABSTRACT Human papillomavirus (HPV) infection is the leading viral cause of cancer. Over the past several decades, research on HPVs has provided remarkable insight into human cell biology and into the pathology of viral and non-viral cancers. The HPV E6 and E7 proteins engage host cellular proteins to establish an environment in infected cells that is conducive to virus replication. They rewire host cell signaling pathways to promote proliferation, inhibit differentiation, and limit cell death. The activity of the “high-risk” HPV E6 and E7 proteins is so potent that their dysregulated expression is sufficient to drive the initiation and maintenance of HPV-associated cancers. Consequently, intensive research efforts have aimed to identify the host cell targets of E6 and E7, in part with the idea that some or all of the virus-host interactions would be essential cancer drivers. These efforts have identified a large number of potential binding partners of each oncoprotein. However, over the same time period, parallel research has revealed that a relatively small number of genetic mutations drive carcinogenesisin most non-viral cancers. We therefore propose that a high-priority goal is to identify which of the many targets of E6 and E7 are critical drivers of HPV carcinogenesis. By identifying the cancer-driving targets of E6 and E7, it should be possible to better understand the distinct roles of other targets, perhaps in the viral life cycle, and to focus efforts to develop anti-cancer therapies on the subset of virus-host interactions for which therapeutic intervention would have the greatest impact.  \nKEYWORDS papillomavirus, carcinogenesis, host-cell interactions, transformation CANCER IS A RARE OUTCOME OF HIGH-RISK HPV INFECTION  \nH uman papillomaviruses (HPVs) are a large family of viruses with small, circular,  \ndouble-stranded DNA genomes of approximately 8,000 base pairs (bp) . Genome sequence diversity is a hallmark of HPVs, and over 400 distinct virus genotypes have been identified. HPVs have a shared tropism for keratinocytes, which are the major constituent of stratified squamous epithelia, and most HPVs share a common genome organization and encode a similar complement of viral genes (1) . Diverse HPVs also share a replication strategy that is closely linked to keratinocyte differentiation (2) . Long-term persistent HPV infection initiates and is maintained in proliferative basal keratinocytes. Subsequent keratinocyte differentiation enables viral genome replication to a high copy number and the production of infectious virions (3) . Although several features of HPV biology are shared among many virus genotypes, the viruses differ in their propensity to infect mucosal or cutaneous epithelia, in the host cell proteins that are targeted by specific HPV-encoded proteins, and in the wide range of pathologies that are associated with HPV infection (1) .  \nInfection with most HPV genotypes causes benign or clinically inapparent lesions, but about a dozen HPVs, including HPV16 and HPV18, are the mucosotropic “high-risk”genotypes that cause lesions that can progress to cancer (4) . Even though cancer is a rare outcome of high-risk HPV infection, the infections are so frequent that they cause at least  \nEditor Vinayaka R. Prasad, Albert Einstein College of Medicine, Bronx, New York, USA  \nAddress correspondence to Karl Munger, [Karl.Munger@tufts.edu](Karl.Munger@tufts.edu), or Elizabeth A. White, [eawhite@pennmedicine.upenn.edu](eawhite@pennmedicine.upenn.edu).  \n5% of all human cancer cases (5) . The mechanisms by which HPV infection initiates or drives carcinogenesis are directly related to features of the HPV life cycle. Persistent HPV infection likely disrupts the normal balance between proliferation and differentiation in infected ","cbCaidEeDdlnwzgv","https://ap.wps.com/l/cbCaidEeDdlnwzgv","pdf",705453,12,"English","# ABSTRACT\n## HPV life cycle and risk of cancer\n## Why E6 and E7 are key drivers","[{\"question\":\"Why is it important to identify which E6 and E7 targets drive cancer?\",\"answer\":\"Many potential binding partners have been identified, but only a subset may be critical drivers. Defining the cancer-driving targets helps clarify the distinct roles of other interactions and supports focusing anti-cancer therapy on the virus-host interfaces with the greatest therapeutic impact.\"}]","What are the essential determinants of human papillomavirus carcinogenesis? - minireview | PDF",1790017383]