Evidence map›Paper›PMID 21734056›Full record

ArticleJournal of virology2011

Suppression of STAT-1 expression by human papillomaviruses is necessary for differentiation-dependent genome amplification and plasmid maintenance.

Shiyuan Hong, Kavi P Mehta, Laimonis A Laimins

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

90 citing papers in PubMed, 119 citations in OpenAlex.

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30 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Shiyuan HongDepartment of Microbiology-Immunology, 303 E. Chicago Ave., Morton 6-681, Chicago, IL 60611, USA.
Kavi P Mehta
Laimonis A Laimins
Northwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-risk human papillomaviruses (HPVs) infect stratified epithelia to establish persistent infections that maintain low-copy-number episomes in infected basal cells. Amplification of viral genomes occurs upon keratinocyte differentiation, followed by virion synthesis. During persistent HPV infections, viral proteins act to evade surveillance by both innate and adaptive immune responses. One of the primary pathways regulating the innate immune response is the JAK/STAT pathway. Our studies indicate that the expression of STAT-1, but not other members of interferon (IFN)-stimulated gene factor 3 (ISGF-3) complex such as STAT-2 and IFN regulatory factor 9 (IRF9), is selectively suppressed by HPV proteins at the level of transcription. Both E6 and E7 oncoproteins independently suppress the expression of STAT-1, and mutational analyses indicate that the E6 targeting E6-associated protein (E6AP) is responsible for suppression. The levels of STAT-1 proteins increase upon differentiation of both normal and HPV-positive cells but are still significantly reduced in the latter cells. Transient restoration of STAT-1 levels in HPV-positive cells using recombinant retroviruses significantly impaired viral amplification upon differentiation while long-term increases abrogated maintenance of episomes. Similarly, increased levels of STAT-1 induced by gamma interferon treatment inhibited HPV genome amplification upon differentiation. Overall, our findings demonstrate that suppression of STAT-1 expression by HPV proteins is necessary for genome amplification and maintenance of episomes, suggesting an important role for this activity in viral pathogenesis.

Indexed as

Host-Pathogen InteractionsVirus ReplicationCells, CulturedHumansImmune EvasionKeratinocytesOncogene Proteins, ViralPapillomaviridaePapillomavirus E7 ProteinsPlasmidsRepressor ProteinsSTAT1 Transcription FactorTranscription, GeneticUbiquitin-Protein LigasesE6 protein, Human papillomavirus type 16oncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsSTAT1 protein, humanSTAT1 Transcription FactorUBE3A protein, humanUbiquitin-Protein Ligases

Identifiers

PMID21734056
PMCPMC3165741
OpenAlexW2125927306

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.