Evidence map›Paper›PMID 23031791›Full record

ArticleVirology journal2012

Inhibition of HCV by the serpin antithrombin III.

Mohammed Asmal, Michael Seaman, Wenyu Lin, Raymond T Chung, Norman L Letvin, Ralf Geiben-Lynn

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Antithrombin and Its Role in Host Defense and Inflammation.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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

6 authors at 4 institutions in 1 country.

Mohammed AsmalDivision of Viral Pathogenesis, BIDMC, Boston, MA 02215, USA. masmal@partners.org
Michael Seaman
Wenyu Lin
Raymond T Chung
Norman L Letvin
Ralf Geiben-Lynn
Beth Israel Deaconess Hospital · USHarvard University · USMassachusetts General Hospital · USMass General Brigham · US

Funding

Viral Sequencing CoreU19AI067854 · NIAID · DUKE UNIVERSITY · PI CRUMP, JOHN ANDREW · 2006 to 2011
$290.5M
The impact of HIV viral diversity and cellular immunity on HIV pathogenesisP30AI060354 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ROBERT A. PARKER · 2004 to 2026
$94.4M
Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F · 2005 to 2005
$14.9M
T CELL MEMORY TO VIRUSESR01AI030048 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AHMED, RAFI · 1990 to 2022
$5.2M
T CELL MEMORY TO VIRUSESR37AI030048 · NIAID · EMORY UNIVERSITY · PI AHMED, RAFI · 2001 to 2010
$3.9M
IN VITRO ANTIVIRAL SCREENING PROGRAM- RESPIRATORY VIRUSES AND BIO DEFENSE PATHOGN01AI30048 · NIAID · UTAH STATE UNIVERSITY · PI SMEE, DONALD F. · 2007 to 2010
$2.0M
In Vitro Antiviral Screening ProgramN01AI30049 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2008 to 2010
$1.8M
NIAID NIH HHS AI060354-06NIAID NIH HHS AI067854NIAID NIH HHS N01 AI30048NIAID NIH HHS N01AI30049
6 · The paper itself

Abstract

backgroundAlthough there have been dramatic strides made recently in the treatment of chronic hepatitis C virus infection, interferon-α based therapy remains challenging for certain populations, including those with unfavorable IL28B genotypes, psychiatric co-morbidity, HIV co-infection, and decompensated liver disease. We have recently shown that ATIII, a serine protease inhibitor (serpin), has broad antiviral properties.

resultsWe now show that ATIII is capable of inhibiting HCV in the OR6 replicon model at micromolar concentrations. At a mechanistic level using gene-expression arrays, we found that ATIII treatment down-regulated multiple host cell signal transduction factors involved in the pathogenesis of cirrhosis and hepatocellular carcinoma, including Jun, Myc and BMP2. Using a protein interactive network analysis we found that changes in gene-expression caused by ATIII were dependent on three nodes previously implicated in HCV disease progression or HCV replication: NFκB, P38 MAPK, and ERK1/2.

conclusionsOur findings suggest that ATIII stimulates a novel innate antiviral host cell defense different from current treatment options.

Indexed as

Antithrombin IIIAntiviral AgentsCell LineGene Expression ProfilingGene Expression RegulationHepacivirusHost-Pathogen InteractionsHumansSignal TransductionVirus ReplicationAntithrombin IIIAntiviral Agents

Identifiers

PMID23031791
PMCPMC3519617
OpenAlexW2155581016

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.