Evidence map›Paper›PMID 30955489›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2019

Cross-talk of cutaneous beta human papillomaviruses and the immune system: determinants of disease penetrance.

Assunta Venuti, Stefan Lohse, Massimo Tommasino, Sigrun Smola

Open access · bronzeAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Targeting innate immunity to overcome immune evasion in HPV-associated cancers.Frontiers in cellular and infection microbiology · 2026
    Review
  3. Clinical and experimental aspects of tirbanibulin treatments.Archives of dermatological research · 2025
    Review
  4. Article
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  18. Towards a multi-level and a multi-disciplinary approach to DNA oncovirus virulence.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    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 2 institutions in 2 countries.

Assunta Venuti1 Infections and Cancer Biology Group, International Agency for Research on Cancer , 150 Cours Albert Thomas, Lyon 69008 , France.
Stefan Lohse2 Institute of Virology, Saarland University Medical Center , Kirrbergerstr. Building 47, 66421 Homburg/Saar , Germany.
Massimo Tommasino1 Infections and Cancer Biology Group, International Agency for Research on Cancer , 150 Cours Albert Thomas, Lyon 69008 , France.
Sigrun Smola2 Institute of Virology, Saarland University Medical Center , Kirrbergerstr. Building 47, 66421 Homburg/Saar , Germany.
Centre international de recherche sur le cancer · FRSaarland University · DE

Funding

World Health Organization 001
6 · The paper itself

Abstract

Human papillomaviruses (HPVs) infect the epithelia of skin or mucosa, where they can induce hyperproliferative lesions. More than 220 different HPV types have been characterized and classified into five different genera. Mucosal high-risk HPVs are causative for cancers of the anogenital region and oropharynx. Clinical data from patients with the rare genetic disorder epidermodysplasia verruciformis (EV) indicate that genus beta-HPVs cooperate with ultraviolet (UV) radiation in the development of cutaneous squamous cell carcinoma. In addition, epidemiological and biological findings indicate that beta-HPV types play a role in UV-mediated skin carcinogenesis also in non-EV individuals. However, the mechanisms used by these cutaneous viruses to promote epithelial carcinogenesis differ significantly from those of mucosal HPVs. Recent studies point to a delicate cross-talk of beta-HPVs with the cell-autonomous immunity of the host keratinocytes and the local immune microenvironment that eventually determines the fate of cutaneous HPV infection and the penetrance of disease. This review gives an overview of the critical interactions of genus beta-HPVs with the local immune system that allow the virus to complete its life cycle, to escape from extrinsic immunity, and eventually to cause chronic inflammation contributing to skin carcinogenesis. This article is part of the theme issue 'Silent cancer agents: multi-disciplinary modelling of human DNA oncoviruses'.

Indexed as

AnimalsBetapapillomavirusDisease SusceptibilityHumansImmune SystemMicePapillomavirus InfectionsSkin Neoplasmsbeta-HPVscutaneous squamous cell carcinomaepidermodysplasia verruciformisimmune systeminflammationorgan transplant recipients

Identifiers

PMID30955489
PMCPMC6501898
OpenAlexW2925780578

What OpenQuestion holds

Textmetadata
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.