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• W2789462012 abstract "first_page settings Order Article Reprints Font Type: Arial Georgia Verdana Font Size: Aa Aa Aa Line Spacing:    Column Width:    Background: Open AccessEditorial Expert Views on HPV Infection by Alison A. McBride 1,* and Karl Münger 2,* 1 Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, 33 North Drive, MSC3209, National Institutes of Health, Bethesda, MD 20892, USA 2 Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA 02111, USA * Authors to whom correspondence should be addressed. Viruses 2018, 10(2), 94; https://doi.org/10.3390/v10020094 Received: 1 February 2018 / Revised: 23 February 2018 / Accepted: 23 February 2018 / Published: 24 February 2018 (This article belongs to the Special Issue Expert Views on HPV Infection) Download Download PDF Download PDF with Cover Download XML Download Epub Versions Notes The goal of this Special Issue was to obtain expert viewpoints on unresolved, controversial or emerging topics related to the natural history, evolution, biology, and disease association of HPV infection. The resulting articles cover a wide range of thought provoking topics.There are over four hundred different papillomavirus (PV) types, which replicate in mucosal and cutaneous stratified epithelial surfaces giving rise to a wide range of lesions. Papillomaviruses have a remarkable life style that relies on the differentiation state of the host epithelium; they infect the basal cells of the epithelium and establish a quiescent infection in the proliferative cells. As the infected cells differentiate, the productive life cycle is activated, and viral-laden squames are eventually released from the surface of the epithelium. To support this life style, PVs interact with, and manipulate, many key cellular pathways. In this Issue, Puustusmaa and colleagues present an intriguing study in which they searched the biosphere for distant homologs of PV protein domains in a quest to discover the origin of papillomaviruses [1]. Suarez and Travé describe insights obtained from a review of PV E6 and E7 structural data [2] and Campos reviews the remarkable abilities of the minor capsid protein L2 to deliver the viral genome to the nucleus upon infection [3]. Moody describes how PVs interface with signaling pathways to provide the virus with a replication-competent environment in differentiating cells [4], and Graham describes how PV late gene expression is regulated by keratinocyte differentiation [5]. MmuPV1, a virus capable of infecting laboratory strains of mice was first described in 2011, and Hu et al. review the remarkable progress made using this valuable model [6]. Over three hundred human papillomavirus (HPV) types have been described and HPV infection is ubiquitous. However, many questions remain about infection, progression and resolution of HPV-associated disease. Gravitt and Weiner present a natural history model across the lifespan of an infected individual, with a particularly focus on the role of viral latency [7]. Alizon and colleagues review our current knowledge about acute/transient infections to provide insight as to why some infections are efficiently cleared while others become persistent [8]. The article by Herfs et al. explains why mucosal junction cells in epithelial transition zones are particularly susceptible to HPV infection and carcinogenic progression [9], while Spurgeon and Lambert describe the role of the stroma and microenvironment in these processes [10]. Continuing in this theme, Strati reviews the role of stem cell dynamics in HPV infection [11]. A subset of alpha-HPVs are oncogenic and are the causative agent of approximately 5% human cancers. Viral manipulation of host pathways can inadvertently promote oncogenesis and several articles in the Special Issue address this. Katzenellenbogen describes the role of telomerase activation in HPV infection and oncogenesis [12], while Warren and colleagues discuss the role of APOBEC3 induction in these processes [13]. Guenat et al. review recent studies showing that HPV regulates the content of exosomes and discuss how this might promote carcinogenesis [14]. Khoury and colleagues explain why the study of HPV infection in individuals prone to cancer due to mutations in DNA repair pathways provides an opportunity to uncover viral and host susceptibility factors [15]. Mirabello et al. report on a meeting of HPV experts that convened to discuss the intersection of HPV epidemiology, genomics and mechanistic studies of HPV-mediated cervical carcinogenesis [16]. Only HPVs from the alpha genus have been officially declared carcinogenic, but there is much discussion about the potential role of beta-HPVs in the initiation of non-melanoma skin cancer. Hufbauer and Akgül describe beta-HPV oncogenic mechanisms that may be relevant for the development of skin cancer [17].HPV-associated cancers acquire profound changes and phenotypes that are important for carcinogenesis and could impact prognosis and treatment. Morgan and colleagues reevaluate the status of integrated and extrachromosomal HPV genomes in head and neck cancer [18] and Litwin et al. review somatic cell mutations that frequently occur in HPV-driven cancers [19]. Soto and colleagues review epigenetic alterations in HPV-associated cancers and explain why these reversible modifications might be amenable to epigenetic therapy [20]. Hoppe-Seyler et al. describe how many HPV-associated cancers have regions of hypoxia containing dormant cancer cells with no viral oncogene expression and explain why this has important consequences for treatment [21]. Finally, two articles review how HPVs modulate factors and pathways important for viral persistence and discuss therapies that could target these key processes. Shanmugasundaram and You describe the mechanisms required for viral genome persistence and discuss how small molecule therapeutics could disrupt this process [22]. Smola reviews the complex interplay between HPV-infected cells and the local immune microenvironment and discusses the potential of related diagnostics and immunotherapies [23]. We thank the authors and reviewers for giving their time, and sharing their expertise, to contribute to this stimulating collection of articles. We hope that the Special Issue has provided insight into many aspects of HPV infection and will inspire future questions, ideas and research. AcknowledgmentsResearch in the McBride laboratory is supported by the Intramural Research Program of the NIAID, NIH and in the Münger laboratory by PHS grant R01 CA066980.ReferencesPuustusmaa, M.; Kirsip, H.; Gaston, K.; Abroi, A. The enigmatic origin of papillomavirus protein domains. Viruses 2017, 9, 240. [Google Scholar] [CrossRef] [PubMed]Suarez, I.; Trave, G. Structural insights in multifunctional papillomavirus oncoproteins. Viruses 2018, 10, 37. [Google Scholar] [CrossRef] [PubMed]Campos, S.K. Subcellular trafficking of the papillomavirus genome during initial infection: The remarkable abilities of minor capsid protein L2. Viruses 2017, 9, 370. [Google Scholar] [CrossRef] [PubMed]Moody, C. Mechanisms by which HPV induces a replication competent environment in differentiating keratinocytes. Viruses 2017, 9, 261. [Google Scholar] [CrossRef] [PubMed]Graham, S.V. Keratinocyte differentiation-dependent human papillomavirus gene regulation. Viruses 2017, 9, 245. [Google Scholar] [CrossRef] [PubMed]Hu, J.; Cladel, N.M.; Budgeon, L.R.; Balogh, K.K.; Christensen, N.D. The mouse papillomavirus infection model. Viruses 2017, 9, 246. [Google Scholar] [CrossRef] [PubMed]Gravitt, P.E.; Winer, R.L. Natural history of HPV infection across the lifespan: Role of viral latency. Viruses 2017, 9, 267. [Google Scholar] [CrossRef] [PubMed]Alizon, S.; Murall, C.L.; Bravo, I.G. Why human papillomavirus acute infections matter. Viruses 2017, 9, 293. [Google Scholar] [CrossRef] [PubMed]Herfs, M.; Soong, T.R.; Delvenne, P.; Crum, C.P. Deciphering the multifactorial susceptibility of mucosal junction cells to HPV infection and related carcinogenesis. Viruses 2017, 9, 85. [Google Scholar] [CrossRef] [PubMed]Spurgeon, M.E.; Lambert, P.F. Human papillomavirus and the stroma: Bidirectional crosstalk during the virus life cycle and carcinogenesis. Viruses 2017, 9, 219. [Google Scholar] [CrossRef] [PubMed]Strati, K. Changing stem cell dynamics during papillomavirus infection: Potential roles for cellular plasticity in the viral lifecycle and disease. Viruses 2017, 9, 221. [Google Scholar] [CrossRef] [PubMed]Katzenellenbogen, R. Telomerase induction in hpv infection and oncogenesis. Viruses 2017, 9, 180. [Google Scholar] [CrossRef] [PubMed]Warren, C.J.; Westrich, J.A.; Doorslaer, K.V.; Pyeon, D. Roles of APOBEC3A and APOBEC3B in human papillomavirus infection and disease progression. Viruses 2017, 9, 233. [Google Scholar] [CrossRef] [PubMed]Guenat, D.; Hermetet, F.; Pretet, J.L.; Mougin, C. Exosomes and other extracellular vesicles in HPV transmission and carcinogenesis. Viruses 2017, 9, 211. [Google Scholar] [CrossRef] [PubMed]Khoury, R.; Sauter, S.; Butsch Kovacic, M.; Nelson, A.; Myers, K.; Mehta, P.; Davies, S.; Wells, S. Risk of human papillomavirus infection in cancer-prone individuals: What we know. Viruses 2018, 10, 47. [Google Scholar] [CrossRef] [PubMed]Mirabello, L.; Clarke, M.A.; Nelson, C.W.; Dean, M.; Wentzensen, N.; Yaeger, M.; Cullen, M.; Boland, J.F.; NCI HPV Wrokshop; Schiffman, M.; et al. The intersection of HPV epidemiology, genomics and mechanistic studies of HPV-mediated carcinogenesis. Viruses 2018, 10, 80. [Google Scholar] [CrossRef] [PubMed]Hufbauer, M.; Akgul, B. Molecular mechanisms of human papillomavirus induced skin carcinogenesis. Viruses 2017, 9, 187. [Google Scholar] [CrossRef] [PubMed]Morgan, I.M.; DiNardo, L.J.; Windle, B. Integration of human papillomavirus genomes in head and neck cancer: Is it time to consider a paradigm shift? Viruses 2017, 9, 208. [Google Scholar] [CrossRef] [PubMed]Litwin, T.R.; Clarke, M.A.; Dean, M.; Wentzensen, N. Somatic host cell alterations in HPV carcinogenesis. Viruses 2017, 9, 206. [Google Scholar] [CrossRef] [PubMed]Soto, D.; Song, C.; McLaughlin-Drubin, M.E. Epigenetic alterations in human papillomavirus-associated cancers. Viruses 2017, 9, 248. [Google Scholar] [CrossRef] [PubMed]Hoppe-Seyler, K.; Mandl, J.; Adrian, S.; Kuhn, B.J.; Hoppe-Seyler, F. Virus/host cell crosstalk in hypoxic HPV-positive cancer cells. Viruses 2017, 9, 174. [Google Scholar] [CrossRef] [PubMed]Shanmugasundaram, S.; You, J. Targeting persistent human papillomavirus infection. Viruses 2017, 9, 229. [Google Scholar] [CrossRef] [PubMed]Smola, S. Immunopathogenesis of HPV-associated cancers and prospects for immunotherapy. Viruses 2017, 9, 254. [Google Scholar] [CrossRef] [PubMed] © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Share and Cite MDPI and ACS Style McBride, A.A.; Münger, K. Expert Views on HPV Infection. Viruses 2018, 10, 94. https://doi.org/10.3390/v10020094 AMA Style McBride AA, Münger K. Expert Views on HPV Infection. Viruses. 2018; 10(2):94. https://doi.org/10.3390/v10020094 Chicago/Turabian Style McBride, Alison A., and Karl Münger. 2018. Expert Views on HPV Infection Viruses 10, no. 2: 94. https://doi.org/10.3390/v10020094 Find Other Styles Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here. Article Metrics No No Article Access Statistics For more information on the journal statistics, click here. 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