Subversion of Host Innate Immunity by Human Papillomavirus Oncoproteins

The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk HPV16/18, to manipulate the signaling pathways involved in cell proliferation, cell death, and innate immunity. Emerging evidence indicates that E6/E...

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Published inPathogens (Basel) Vol. 9; no. 4; p. 292
Main Authors Lo Cigno, Irene, Calati, Federica, Albertini, Silvia, Gariglio, Marisa
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 17.04.2020
MDPI
Subjects
Adenosine
Apoptosis
Cancer
Cell cycle
Cell death
Cell proliferation
Cervical cancer
Chemotherapy
Cytokines
Deoxyribonucleic acid
Depletion
DNA
E6 and E7 oncoproteins
Gene expression
Genomes
HPV
HPV-driven cancer
Human papillomavirus
Immune response
Immune system
Immunity
Infections
Innate immunity
Interferon
Literature reviews
Oncoproteins
pathogen recognition receptors
Pathogens
Proteins
Review
Signal transduction
Signaling
Target recognition
Therapeutic applications
Toll-like receptors
Transformed cells
Tumorigenesis
Tumors
Vaccines
PRR
innate immunity
human papillomavirus
pathogen recognition receptors
E6 and E7 oncoproteins
HPV
HPV-driven cancer
Online AccessGet full text
ISSN2076-0817
2076-0817
DOI10.3390/pathogens9040292

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Abstract The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk HPV16/18, to manipulate the signaling pathways involved in cell proliferation, cell death, and innate immunity. Emerging evidence indicates that E6/E7 inhibition reactivates the host innate immune response, reversing what until then was an unresponsive cellular state suitable for viral persistence and tumorigenesis. Given that the disruption of distinct mechanisms of immune evasion is an attractive strategy for cancer therapy, the race is on to gain a better understanding of E6/E7-induced immune escape and cancer progression. Here, we review recent literature on the interplay between E6/E7 and the innate immune signaling pathways cGAS/STING/TBK1, RIG-I/MAVS/TBK1, and Toll-like receptors (TLRs). The overall emerging picture is that E6 and E7 have evolved broad-spectrum mechanisms allowing for the simultaneous depletion of multiple rather than single innate immunity effectors. The cGAS/STING/TBK1 pathway appears to be the most heavily impacted, whereas the RIG-I/MAVS/TBK1, still partially functional in HPV-transformed cells, can be activated by the powerful RIG-I agonist M8, triggering the massive production of type I and III interferons (IFNs), which potentiates chemotherapy-mediated cell killing. Overall, the identification of novel therapeutic targets to restore the innate immune response in HPV-transformed cells could transform the way HPV-associated cancers are treated.
AbstractList The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk HPV16/18, to manipulate the signaling pathways involved in cell proliferation, cell death, and innate immunity. Emerging evidence indicates that E6/E7 inhibition reactivates the host innate immune response, reversing what until then was an unresponsive cellular state suitable for viral persistence and tumorigenesis. Given that the disruption of distinct mechanisms of immune evasion is an attractive strategy for cancer therapy, the race is on to gain a better understanding of E6/E7-induced immune escape and cancer progression. Here, we review recent literature on the interplay between E6/E7 and the innate immune signaling pathways cGAS/STING/TBK1, RIG-I/MAVS/TBK1, and Toll-like receptors (TLRs). The overall emerging picture is that E6 and E7 have evolved broad-spectrum mechanisms allowing for the simultaneous depletion of multiple rather than single innate immunity effectors. The cGAS/STING/TBK1 pathway appears to be the most heavily impacted, whereas the RIG-I/MAVS/TBK1, still partially functional in HPV-transformed cells, can be activated by the powerful RIG-I agonist M8, triggering the massive production of type I and III interferons (IFNs), which potentiates chemotherapy-mediated cell killing. Overall, the identification of novel therapeutic targets to restore the innate immune response in HPV-transformed cells could transform the way HPV-associated cancers are treated.
The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk HPV16/18, to manipulate the signaling pathways involved in cell proliferation, cell death, and innate immunity. Emerging evidence indicates that E6/E7 inhibition reactivates the host innate immune response, reversing what until then was an unresponsive cellular state suitable for viral persistence and tumorigenesis. Given that the disruption of distinct mechanisms of immune evasion is an attractive strategy for cancer therapy, the race is on to gain a better understanding of E6/E7-induced immune escape and cancer progression. Here, we review recent literature on the interplay between E6/E7 and the innate immune signaling pathways cGAS/STING/TBK1, RIG-I/MAVS/TBK1, and Toll-like receptors (TLRs). The overall emerging picture is that E6 and E7 have evolved broad-spectrum mechanisms allowing for the simultaneous depletion of multiple rather than single innate immunity effectors. The cGAS/STING/TBK1 pathway appears to be the most heavily impacted, whereas the RIG-I/MAVS/TBK1, still partially functional in HPV-transformed cells, can be activated by the powerful RIG-I agonist M8, triggering the massive production of type I and III interferons (IFNs), which potentiates chemotherapy-mediated cell killing. Overall, the identification of novel therapeutic targets to restore the innate immune response in HPV-transformed cells could transform the way HPV-associated cancers are treated.The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk HPV16/18, to manipulate the signaling pathways involved in cell proliferation, cell death, and innate immunity. Emerging evidence indicates that E6/E7 inhibition reactivates the host innate immune response, reversing what until then was an unresponsive cellular state suitable for viral persistence and tumorigenesis. Given that the disruption of distinct mechanisms of immune evasion is an attractive strategy for cancer therapy, the race is on to gain a better understanding of E6/E7-induced immune escape and cancer progression. Here, we review recent literature on the interplay between E6/E7 and the innate immune signaling pathways cGAS/STING/TBK1, RIG-I/MAVS/TBK1, and Toll-like receptors (TLRs). The overall emerging picture is that E6 and E7 have evolved broad-spectrum mechanisms allowing for the simultaneous depletion of multiple rather than single innate immunity effectors. The cGAS/STING/TBK1 pathway appears to be the most heavily impacted, whereas the RIG-I/MAVS/TBK1, still partially functional in HPV-transformed cells, can be activated by the powerful RIG-I agonist M8, triggering the massive production of type I and III interferons (IFNs), which potentiates chemotherapy-mediated cell killing. Overall, the identification of novel therapeutic targets to restore the innate immune response in HPV-transformed cells could transform the way HPV-associated cancers are treated.
Author Calati, Federica
Lo Cigno, Irene
Albertini, Silvia
Gariglio, Marisa
AuthorAffiliation Molecular Virology Unit, Department of Translational Medicine, Medical School, University of Piemonte Orientale, 28100 Novara, Italy; irene.locigno@med.uniupo.it (I.L.C.); federica.calati@med.uniupo.it (F.C.); silvia.albertini@med.uniupo.it (S.A.)
AuthorAffiliation_xml – name: Molecular Virology Unit, Department of Translational Medicine, Medical School, University of Piemonte Orientale, 28100 Novara, Italy; irene.locigno@med.uniupo.it (I.L.C.); federica.calati@med.uniupo.it (F.C.); silvia.albertini@med.uniupo.it (S.A.)
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  orcidid: 0000-0001-5521-3642
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  fullname: Lo Cigno, Irene
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  surname: Calati
  fullname: Calati, Federica
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  surname: Albertini
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  surname: Gariglio
  fullname: Gariglio, Marisa
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Keywords PRR
innate immunity
human papillomavirus
pathogen recognition receptors
E6 and E7 oncoproteins
HPV
HPV-driven cancer
Language English
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Snippet The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk...
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SubjectTerms Adenosine
Apoptosis
Cancer
Cell cycle
Cell death
Cell proliferation
Cervical cancer
Chemotherapy
Cytokines
Deoxyribonucleic acid
Depletion
DNA
E6 and E7 oncoproteins
Gene expression
Genomes
HPV
HPV-driven cancer
Human papillomavirus
Immune response
Immune system
Immunity
Infections
Innate immunity
Interferon
Literature reviews
Oncoproteins
pathogen recognition receptors
Pathogens
Proteins
Review
Signal transduction
Signaling
Target recognition
Therapeutic applications
Toll-like receptors
Transformed cells
Tumorigenesis
Tumors
Vaccines
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Title Subversion of Host Innate Immunity by Human Papillomavirus Oncoproteins
URI https://www.ncbi.nlm.nih.gov/pubmed/32316236
https://www.proquest.com/docview/2392881303
https://www.proquest.com/docview/2393573569
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https://doaj.org/article/72c250d690ba4e6691cdc19d8c594fdb
Volume 9
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