Evidence map›Paper›PMID 30616034›Full record

ReviewCytokine2019

Decoding the enigma of antiviral crisis: Does one target molecule regulate all?

Abdullah Mahmud-Al-Rafat, Apurba Majumder, K M Taufiqur Rahman, A M Mahedi Hasan, K M Didarul Islam, Andrew W Taylor-Robinson, Md Morsaline Billah

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.9field-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

21 citing papers in PubMed, 36 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

7 authors at 5 institutions in 5 countries.

Abdullah Mahmud-Al-RafatResearch & Development Division, Incepta Vaccine Ltd., Zirabo, Savar, Dhaka 1341, Bangladesh; Biotechnology and Genetic Engineering Discipline, Khulna University, Khulna 9208, Bangladesh. Electronic address: mahmud0907@gmail.com.
Apurba MajumderDepartment of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover 30625, Germany.
K M Taufiqur RahmanDepartment of Chemistry and Biomolecular Sciences, University of Ottawa, Ottawa, Ontario K1N6N5, Canada. Electronic address: krahm066@uottawa.ca.
A M Mahedi HasanInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FF, UK. Electronic address: A.M.M.Hasan@ed.ac.uk.
K M Didarul IslamBiotechnology and Genetic Engineering Discipline, Khulna University, Khulna 9208, Bangladesh.
Andrew W Taylor-RobinsonSchool of Health, Medical & Applied Sciences, Central Queensland University, Brisbane, QLD 4000, Australia. Electronic address: a.taylor-robinson@cqu.edu.au.
Md Morsaline BillahBiotechnology and Genetic Engineering Discipline, Khulna University, Khulna 9208, Bangladesh. Electronic address: morsaline@yahoo.com.
Khulna University · BDCentral Queensland University · AUMedizinische Hochschule Hannover · DEUniversity of Edinburgh · GBUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disease fatality associated with Ebola, SARS-CoV and dengue infections in humans is attributed to a cytokine storm that is triggered by excessive pro-inflammatory responses. Interleukin (IL)-6 acts as a mediator between pro- and anti-inflammatory reactivity by initiating trans- and classical-signaling, respectively. Hence, IL-6 is assumed to provide a target for a broad range of antiviral agents. Available immunosuppressive antivirals are directed to control an often exaggerated pro-inflammatory response that gives rise to complex clinical conditions such as lymphocytopenia. It is known that IL-6, via its soluble receptor (sIL-6R), initiates a pro-inflammatory response while an anti-inflammatory response is triggered by the membrane-bound IL-6 receptor (IL-6R). Future antivirals should thus aim to target the mechanism that regulates switching between IL-6 trans- and classical-signaling. In this review, we propose that the tumour necrosis factor-α converting enzyme ADAM-17 could be the master molecule involved in regulating IL-6 class switching and through this in controlling pro- and anti-inflammatory responses to viral antigenic stimuli. Therefore, ADAM-17 should be considered as a potential target molecule for novel antiviral drug discovery that would regulate host reactivity to infection and thereby limit or prevent fatal outcomes.

Indexed as

ADAM17 ProteinAnimalsAntiviral AgentsHumansImmunosuppressive AgentsInflammationInterleukin-6Receptors, Interleukin-6Signal TransductionADAM17 ProteinAntiviral AgentsImmunosuppressive AgentsInterleukin-6Receptors, Interleukin-6ADAM-17AntiviralCytokine stormDengueEbolaIL-6Pro-inflammatory responseSARS-CoVVirus

Identifiers

PMID30616034
PMCPMC7129598
OpenAlexW2908095133

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.