Evidence map›Paper›PMID 32316236›Full record

ReviewPathogens (Basel, Switzerland)2020

Subversion of Host Innate Immunity by Human Papillomavirus Oncoproteins.

Irene Lo Cigno, Federica Calati, Silvia Albertini, Marisa Gariglio

Open access · goldAbstract readReview
In one paragraph

Review in Pathogens (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Targeting innate immunity to overcome immune evasion in HPV-associated cancers.Frontiers in cellular and infection microbiology · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Targeted degradation of the HPV oncoprotein E6 reduces tumor burden in cervical cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Irene Lo CignoMolecular Virology Unit, Department of Translational Medicine, Medical School, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0001-5521-3642
Federica CalatiMolecular Virology Unit, Department of Translational Medicine, Medical School, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-8830-8290
Silvia AlbertiniMolecular Virology Unit, Department of Translational Medicine, Medical School, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-8540-5378
Marisa GariglioMolecular Virology Unit, Department of Translational Medicine, Medical School, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-5187-0140
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

Associazione Italiana per la Ricerca sul Cancro IG2016 grant to M.GMinistero dell'Istruzione, dell'Università e della Ricerca AGING Project - Department of Excellence - Department of Translational Medicine, University of Piemonte OrientaleMinistero dell'Istruzione, dell'Università e della Ricerca PRIN 2017 to M.G
6 · The paper itself

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.

Indexed as

E6 and E7 oncoproteinsHPVHPV-driven cancerhuman papillomavirusinnate immunitypathogen recognition receptorsPRR

Identifiers

PMID32316236
PMCPMC7238203
OpenAlexW3016738221

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.