Evidence map›Paper›PMID 29257060›Full record

ReviewViruses2017

How Human Papillomavirus Replication and Immune Evasion Strategies Take Advantage of the Host DNA Damage Repair Machinery.

Valentina Bordignon, Enea Gino Di Domenico, Elisabetta Trento, Giovanna D'Agosto, Ilaria Cavallo, Martina Pontone, Fulvia Pimpinelli, Luciano Mariani, Fabrizio Ensoli

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Valentina BordignonClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. valentina.bordignon@ifo.gov.it.
Enea Gino Di DomenicoClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. enea.didomenico@ifo.gov.it.ORCID 0000-0001-6295-6006
Elisabetta TrentoClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. elisabetta.trento@ifo.gov.it.
Giovanna D'AgostoClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. giovanna.dagosto@ifo.gov.it.
Ilaria CavalloClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. ilaria.cavallo90@gmail.com.
Martina PontoneClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. martina.pontone@ifo.gov.it.
Fulvia PimpinelliClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. fulvia.pimpinelli@ifo.gov.it.
Luciano MarianiHPV Unit, Department of Gynaecologic Oncology, National Cancer Institute Regina Elena, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. luciano.mariani@ifo.gov.it.
Fabrizio EnsoliClinical Pathology and Microbiology Unit, San Gallicano Dermatology Institute, IRCCS, IFO, Via Elio Chianesi 53, 00144 Rome, Italy. fabrizio.ensoli@ifo.gov.it.
San Gallicano Hospital · ITIstituti Fisioterapici Ospitalieri · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA damage response (DDR) is a complex signalling network activated when DNA is altered by intrinsic or extrinsic agents. DDR plays important roles in genome stability and cell cycle regulation, as well as in tumour transformation. Viruses have evolved successful life cycle strategies in order to ensure a chronic persistence in the host, virtually avoiding systemic sequelae and death. This process promotes the periodic shedding of large amounts of infectious particles to maintain a virus reservoir in individual hosts, while allowing virus spreading within the community. To achieve such a successful lifestyle, the human papilloma virus (HPV) needs to escape the host defence systems. The key to understanding how this is achieved is in the virus replication process that provides by itself an evasion mechanism by inhibiting and delaying the host immune response against the viral infection. Numerous studies have demonstrated that HPV exploits both the ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia and rad3-related (ATR) DDR pathways to replicate its genome and maintain a persistent infection by downregulating the innate and cell-mediated immunity. This review outlines how HPV interacts with the ATM- and ATR-dependent DDR machinery during the viral life cycle to create an environment favourable to viral replication, and how the interaction with the signal transducers and activators of transcription (STAT) protein family and the deregulation of the Janus kinase (JAK)-STAT pathways may impact the expression of interferon-inducible genes and the innate immune responses.

Indexed as

Host-Pathogen InteractionsImmune EvasionVirus ReplicationAnimalsDNA Repair EnzymesHumansPapillomaviridaeDNA Repair EnzymesATMATRDNA damage repair (DDR)human papillomavirus (HPV)IFN-γSTAT-5viral immune evasion

Identifiers

PMID29257060
PMCPMC5744164
OpenAlexW2778876312

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.