Evidence map›Paper›PMID 28794024›Full record

ArticleJournal of virology2017

Highly Pathogenic New World Arenavirus Infection Activates the Pattern Recognition Receptor Protein Kinase R without Attenuating Virus Replication in Human Cells.

Cheng Huang, Olga A Kolokoltsova, Elizabeth J Mateer, Takaaki Koma, Slobodan Paessler

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 31 citations in OpenAlex.

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  11. Ribosomal control in RNA virus-infected cells.Frontiers in microbiology · 2022
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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

5 authors at 1 institution in 1 country.

Cheng HuangDepartment of Pathology and Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA chhuang@utmb.edu slpaessl@utmb.edu.
Olga A KolokoltsovaDepartment of Pathology and Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA.
Elizabeth J MateerDepartment of Pathology and Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA.
Takaaki KomaDepartment of Pathology and Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA.
Slobodan PaesslerDepartment of Pathology and Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA chhuang@utmb.edu slpaessl@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

Recombinant life attenuated vaccine against Argentine hemorrhagic feverR01AI093445 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI DE LA TORRE, JUAN C., PAESSLER, SLOBODAN · 2011 to 2015
$4.6M
NIAID NIH HHS R01 AI093445
6 · The paper itself

Abstract

The arenavirus family consists of several highly pathogenic viruses, including the Old World (OW) arenavirus Lassa fever virus (LASV) and the New World (NW) Junin virus (JUNV) and Machupo virus (MACV). Host response to infection by these pathogenic arenaviruses is distinct in many aspects. JUNV and MACV infections readily induce an interferon (IFN) response in human cells, while LASV infection usually triggers an undetectable or weak IFN response. JUNV induces an IFN response through RIG-I, suggesting that the host non-self RNA sensor readily detects JUNV viral RNAs (vRNAs) during infection and activates IFN response. Double-stranded-RNA (dsRNA)-activated protein kinase R (PKR) is another host non-self RNA sensor classically known for its vRNA recognition activity. Here we report that infection with NW arenaviruses JUNV and MACV, but not OW LASV, activated PKR, concomitant with elevated phosphorylation of the translation initiation factor α subunit of eukaryotic initiation factor 2 (eIF2α). Host protein synthesis was substantially suppressed in MACV- and JUNV-infected cells but was only marginally reduced in LASV-infected cells. Despite the antiviral activity known for PKR against many other viruses, the replication of JUNV and MACV was not impaired but was slightly augmented in wild-type (wt) cells compared to that in PKR-deficient cells, suggesting that PKR or PKR activation did not negatively affect JUNV and MACV infection. Additionally, we found an enhanced IFN response in JUNV- or MACV-infected PKR-deficient cells, which was inversely correlated with virus replication.

Indexed as

Immunity, InnateVirus ReplicationA549 CellsArenaviruses, New WorldArenaviruses, Old WorldeIF-2 KinaseHost-Pathogen InteractionsHumansInterferonsJunin virusPhosphorylationReceptors, Pattern RecognitionTranscription FactorsEIF2AK2 protein, humaneIF-2 KinaseELF2 protein, humanInterferonsReceptors, Pattern RecognitionTranscription Factorsarenavirushost-pathogen interactionsinnate immune responseinterferonsPKR

Identifiers

PMID28794024
PMCPMC5625494
OpenAlexW2743460110

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.