Evidence map›Paper›PMID 30146782›Full record

ReviewJournal of cellular physiology2019

Modulation of the immune response by Middle East respiratory syndrome coronavirus.

Somayeh Shokri, Shahab Mahmoudvand, Reza Taherkhani, Fatemeh Farshadpour

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

55 citing papers in PubMed, 97 citations in OpenAlex.

  1. Trial
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  10. Yoga, immunity and COVID-19: A scoping review.Journal of family medicine and primary care · 2022
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  15. Lessons from SARS-CoV, MERS-CoV, and SARS-CoV-2 Infections: What We Know So Far.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2022
    Review
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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

4 authors at 2 institutions in 1 country.

Somayeh ShokriStudent Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Shahab MahmoudvandStudent Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Reza TaherkhaniThe Persian Gulf Tropical Medicine Research Center, Bushehr University of Medical Sciences, Bushehr, Iran.
Fatemeh FarshadpourThe Persian Gulf Tropical Medicine Research Center, Bushehr University of Medical Sciences, Bushehr, Iran.ORCID 0000-0002-8317-9573
Ahvaz Jundishapur University of Medical Sciences · IRBushehr University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus (CoV) infections are commonly associated with respiratory and enteric disease in humans and animals. In 2012, a new human disease called Middle East respiratory syndrome (MERS) emerged in the Middle East. MERS was caused by a virus that was originally called human coronavirus-Erasmus Medical Center/2012 but was later renamed as Middle East respiratory syndrome coronavirus (MERS-CoV). MERS-CoV causes high fever, cough, acute respiratory tract infection, and multiorgan dysfunction that may eventually lead to the death of the infected individuals. The exact origin of MERS-CoV remains unknown, but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host, from which human infections may sporadically occur through the zoonotic transmission. Human to human transmission also occurs in healthcare facilities and communities. Recent studies on Middle Eastern respiratory continue to highlight the need for further understanding the virus-host interactions that govern disease severity and infection outcome. In this review, we have highlighted the major mechanisms of immune evasion strategies of MERS-CoV. We have demonstrated that M, 4a, 4b proteins and Plppro of MERS-CoV inhibit the type I interferon (IFN) and nuclear factor-κB signaling pathways and therefore facilitate innate immune evasion. In addition, nonstructural protein 4a (NSP4a), NSP4b, and NSP15 inhibit double-stranded RNA sensors. Therefore, the mentioned proteins limit early induction of IFN and cause rapid apoptosis of macrophages. MERS-CoV strongly inhibits the activation of T cells with downregulation of antigen presentation. In addition, uncontrolled secretion of interferon ɣ-induced protein 10 and monocyte chemoattractant protein-1 can suppress proliferation of human myeloid progenitor cells.

Indexed as

Coronavirus InfectionsHost-Pathogen InteractionsHumansImmune EvasionImmunity, InnateMiddle East Respiratory Syndrome Coronavirusimmune evasionimmune responseMiddle East respiratory syndrome coronavirus

Identifiers

PMID30146782
PMCPMC7166610
OpenAlexW2889462389

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.