Evidence map›Paper›PMID 25262851›Full record

ReviewVirus research2014

Modulation of innate immune signaling by nonstructural protein 1 (nsp1) in the family Arteriviridae.

Mingyuan Han, Dongwan Yoo

Open access · greenAbstract readReview
In one paragraph

Review in Virus research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 42 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

2 authors at 1 institution in 1 country.

Mingyuan HanDepartment of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61802, USA.
Dongwan YooDepartment of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61802, USA. Electronic address: dyoo@illinois.edu.
University of Illinois Urbana-Champaign · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arteriviruses infect immune cells and may cause persistence in infected hosts. Inefficient induction of pro-inflammatory cytokines and type I IFNs are observed during infection of this group of viruses, suggesting that they may have evolved to escape the host immune surveillance for efficient survival. Recent studies have identified viral proteins regulating the innate immune signaling, and among these, nsp1 (nonstructural protein 1) is the most potent IFN antagonist. For porcine reproductive and respiratory syndrome virus (PRRSV), individual subunits (nsp1α and nsp1β) of nsp1 suppress type I IFN production. In particular, PRRSV-nsp1α degrades CREB (cyclic AMP responsive element binding)-binding protein (CBP), a key component of the IFN enhanceosome, whereas PRRSV-nsp1β degrades karyopherin-α1 which is known to mediate the nuclear import of ISGF3 (interferon-stimulated gene factor 3). All individual subunits of nsp1 of PRRSV, equine arteritis virus (EAV), lactate dehydrogenase-elevating virus (LDV), and simian hemorrhagic fever virus (SHFV) appear to contain IFN suppressive activities. As with PRRSV-nsp1α, CBP degradation is evident by LDV-nsp1α and partly by SHFV-nsp1γ. This review summarizes the biogenesis and the role of individual subunits of nsp1 of arteriviruses for innate immune modulation.

Indexed as

Host-Pathogen InteractionsImmune EvasionImmunity, InnateArterivirusInterferon Type IViral Nonstructural ProteinsInterferon Type IViral Nonstructural ProteinsArterivirusCREB-binding proteinInnate immunityInterferon signalingnsp1PRRSV

Identifiers

PMID25262851
PMCPMC7114407
OpenAlexW2001947268

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.