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Viruses
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Recent Advances in Papillomaviruses Research
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Recent Advances in Papillomaviruses Research

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 18544

Special Issue Editors

Prof. Dr. Thomas Iftner

E-Mail Website
Guest Editor
Institute of Medical Virology, Universität Tübingen, Tubingen, Germany
Interests: papillomaviruses
Dr. Frank Stubenrauch

E-Mail Website
Guest Editor
Institute of Medical Virology, Universität Tübingen, Tubingen, Germany
Interests: papillomaviruses

Special Issue Information

Dear Colleagues,

Persistent infections with high risk human papillomaviruses (HPV) account for more than 600.000 newly diagnosed cancers of the anogenital and oropharyngeal tract annually. Although much information has been gathered from laboratory and clinical investigations, we still have an incomplete picture of the critical interactions of HPV with host cells and the immune system. This Special Issue on Recent Advances in Papillomaviruses Research in Viruses will provide a multifaceted view of the latest research into papillomaviruses. Each chapter in this series will highlight the efforts and progress made to acquire basic knowledge of HPV host interactions and will indicate particular areas that remain to be uncovered. Topics in this new series include the processes of HPV entry into keratinocytes, HPV and the DNA damage response, BRD4 proteins in the HPV life cycle, different animal papillomavirus model systems as well as updates on L2- based prophylactic vaccines and on improved HPV diagnostics.

Prof. Dr. Thomas Iftner
Prof. Dr. Frank Stubenrauch
Guest Editors

Keywords

  • papillomavirus
  • virus entry
  • DNA Damage response
  • vaccine
  • virus-host-interaction
  • HPV diagnostics
  • cancer
  • animal models

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Published Papers (5 papers)

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Research

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17 pages, 2930 KiB  
Article
HPV16 Induces Formation of Virus-p62-PML Hybrid Bodies to Enable Infection
by Linda Schweiger, Laura A. Lelieveld-Fast, Snježana Mikuličić, Johannes Strunk, Kirsten Freitag, Stefan Tenzer, Albrecht M. Clement and Luise Florin
Viruses 2022, 14(7), 1478; https://doi.org/10.3390/v14071478 - 5 Jul 2022
Cited by 6 | Viewed by 2792
Abstract
Human papillomaviruses (HPVs) inflict a significant burden on the human population. The clinical manifestations caused by high-risk HPV types are cancers at anogenital sites, including cervical cancer, as well as head and neck cancers. Host cell defense mechanisms such as autophagy are initiated [...] Read more.
Human papillomaviruses (HPVs) inflict a significant burden on the human population. The clinical manifestations caused by high-risk HPV types are cancers at anogenital sites, including cervical cancer, as well as head and neck cancers. Host cell defense mechanisms such as autophagy are initiated upon HPV entry. At the same time, the virus modulates cellular antiviral processes and structures such as promyelocytic leukemia nuclear bodies (PML NBs) to enable infection. Here, we uncover the autophagy adaptor p62, also known as p62/sequestosome-1, as a novel proviral factor in infections by the high-risk HPV type 16 (HPV16). Proteomics, imaging and interaction studies of HPV16 pseudovirus-treated HeLa cells display that p62 is recruited to virus-filled endosomes, interacts with incoming capsids, and accompanies the virus to PML NBs, the sites of viral transcription and replication. Cellular depletion of p62 significantly decreased the delivery of HPV16 viral DNA to PML NBs and HPV16 infection rate. Moreover, the absence of p62 leads to an increase in the targeting of viral components to autophagic structures and enhanced degradation of the viral capsid protein L2. The proviral role of p62 and formation of virus-p62-PML hybrid bodies have also been observed in human primary keratinocytes, the HPV target cells. Together, these findings suggest the previously unrecognized virus-induced formation of p62-PML hybrid bodies as a viral mechanism to subvert the cellular antiviral defense, thus enabling viral gene expression. Full article
(This article belongs to the Special Issue Recent Advances in Papillomaviruses Research)
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11 pages, 1735 KiB  
Article
The E6 Oncoprotein of HPV16 AA-c Variant Regulates Cell Migration through the MINCR/miR-28-5p/RAP1B Axis
by Eduardo Gil Perez-Bacho, Fredy Omar Beltrán-Anaya, Elena Arechaga-Ocampo, Daniel Hernández-Sotelo, Olga Lilia Garibay-Cerdenares, Berenice Illades-Aguiar, Luz Del Carmen Alarcón-Romero and Oscar Del Moral-Hernández
Viruses 2022, 14(5), 963; https://doi.org/10.3390/v14050963 - 5 May 2022
Cited by 6 | Viewed by 2584
Abstract
The E6 oncoprotein of HPV16 variants differentially alters the transcription of the genes involved in migration and non-coding RNAs such as lncRNAs. The role of the lncRNA MINCR in cervical cancer and its relationship with variants of oncogenic HPV remain unknown. Therefore, the [...] Read more.
The E6 oncoprotein of HPV16 variants differentially alters the transcription of the genes involved in migration and non-coding RNAs such as lncRNAs. The role of the lncRNA MINCR in cervical cancer and its relationship with variants of oncogenic HPV remain unknown. Therefore, the objective of this study was to analyze the effect of the E6 oncoprotein of the AA-c variant of HPV16 in cell migration through the MINCR/miR-28-5p/RAP1B axis. To explore the functional role of MINCR in CC, we used an in vitro model of C33-A cells with exogenous expression of the E6 oncoprotein of the AA-c variant of HPV16. Interfering RNAs performed MINCR silencing, and the expression of miR-28-5p and RAP1B mRNA was analyzed by RT-qPCR. We found that C33-A/AA-c cells expressed MINCR 8-fold higher compared to the control cells. There is an inverse correlation between the expression of miR-28-5p and RAP1B in C33-A/AA-c cells. Our results suggest that MINCR might regulate the expression of RAP1B through the inhibition of miR-28-5p in CC cells expressing the E6 oncoprotein of HPV16 AA-c. We report, for the first time, that the MINCR/miR-28-5p/RAP1B axis positively regulates cell migration in CC-derived cells that express the E6 oncoprotein of the AA-c variant of HPV16. Full article
(This article belongs to the Special Issue Recent Advances in Papillomaviruses Research)
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Review

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10 pages, 1240 KiB  
Review
Functions of Papillomavirus E8^E2 Proteins in Tissue Culture and In Vivo
by Franziska Kuehner and Frank Stubenrauch
Viruses 2022, 14(5), 953; https://doi.org/10.3390/v14050953 - 2 May 2022
Cited by 5 | Viewed by 2463
Abstract
Papillomaviruses (PV) replicate in undifferentiated keratinocytes at low levels and to high levels in differentiated cells. The restricted replication in undifferentiated cells is mainly due to the expression of the conserved viral E8^E2 repressor protein, a fusion protein consisting of E8 and the [...] Read more.
Papillomaviruses (PV) replicate in undifferentiated keratinocytes at low levels and to high levels in differentiated cells. The restricted replication in undifferentiated cells is mainly due to the expression of the conserved viral E8^E2 repressor protein, a fusion protein consisting of E8 and the hinge, DNA-binding, and dimerization domain of E2. E8^E2 binds to viral genomes and represses viral transcription and genome replication by recruiting cellular NCoR/SMRT-HDAC3 corepressor complexes. Tissue culture experiments have revealed that E8^E2 modulates long-term maintenance of extrachromosomal genomes, productive replication, and immortalization properties in a virus type-dependent manner. Furthermore, in vivo experiments have indicated that Mus musculus PV1 E8^E2 is required for tumor formation in immune-deficient mice. In summary, E8^E2 is a crucial inhibitor whose levels might determine the outcome of PV infections. Full article
(This article belongs to the Special Issue Recent Advances in Papillomaviruses Research)
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16 pages, 6994 KiB  
Review
HPV16 Entry into Epithelial Cells: Running a Gauntlet
by Snježana Mikuličić, Johannes Strunk and Luise Florin
Viruses 2021, 13(12), 2460; https://doi.org/10.3390/v13122460 - 8 Dec 2021
Cited by 11 | Viewed by 5390
Abstract
During initial infection, human papillomaviruses (HPV) take an unusual trafficking pathway through their host cell. It begins with a long period on the cell surface, during which the capsid is primed and a virus entry platform is formed. A specific type of clathrin-independent [...] Read more.
During initial infection, human papillomaviruses (HPV) take an unusual trafficking pathway through their host cell. It begins with a long period on the cell surface, during which the capsid is primed and a virus entry platform is formed. A specific type of clathrin-independent endocytosis and subsequent retrograde trafficking to the trans-Golgi network follow this. Cellular reorganization processes, which take place during mitosis, enable further virus transport and the establishment of infection while evading intrinsic cellular immune defenses. First, the fragmentation of the Golgi allows the release of membrane-encased virions, which are partially protected from cytoplasmic restriction factors. Second, the nuclear envelope breakdown opens the gate for these virus–vesicles to the cell nucleus. Third, the dis- and re-assembly of the PML nuclear bodies leads to the formation of modified virus-associated PML subnuclear structures, enabling viral transcription and replication. While remnants of the major capsid protein L1 and the viral DNA remain in a transport vesicle, the viral capsid protein L2 plays a crucial role during virus entry, as it adopts a membrane-spanning conformation for interaction with various cellular proteins to establish a successful infection. In this review, we follow the oncogenic HPV type 16 during its long journey into the nucleus, and contrast pro- and antiviral processes. Full article
(This article belongs to the Special Issue Recent Advances in Papillomaviruses Research)
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16 pages, 1446 KiB  
Review
Human Papillomaviruses Target the DNA Damage Repair and Innate Immune Response Pathways to Allow for Persistent Infection
by Elona Gusho and Laimonis Laimins
Viruses 2021, 13(7), 1390; https://doi.org/10.3390/v13071390 - 17 Jul 2021
Cited by 18 | Viewed by 4327
Abstract
Persistent infection with high-risk human papillomaviruses (HPVs) is the major risk factor associated with development of anogenital and oropharyngeal cancers. Initial infection by HPVs occurs into basal epithelial cells where viral genomes are established as nuclear episomes and persist until cleared by the [...] Read more.
Persistent infection with high-risk human papillomaviruses (HPVs) is the major risk factor associated with development of anogenital and oropharyngeal cancers. Initial infection by HPVs occurs into basal epithelial cells where viral genomes are established as nuclear episomes and persist until cleared by the immune response. Productive replication or amplification occurs upon differentiation and is dependent upon activation of the ataxia-telangiectasia mutated (ATM), ataxia telangiectasia and RAD3-related (ATR) DNA damage repair (DDR) pathways. In addition to activating DDR pathways, HPVs must escape innate immune surveillance mechanisms by antagonizing sensors, adaptors, interferons and antiviral gene expression. Both DDR and innate immune pathways are key host mechanisms that crosstalk with each other to maintain homeostasis of cells persistently infected with HPVs. Interestingly, it is still not fully understood why some HPV infections get cleared while others do not. Targeting of these two processes with antiviral therapies may provide opportunities for treatment of cancers caused by high-risk HPVs. Full article
(This article belongs to the Special Issue Recent Advances in Papillomaviruses Research)
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