Evidence map›Paper›PMID 35818398›Full record

ArticleInformatics in medicine unlocked2022

Systems biology models to identify the influence of SARS-CoV-2 infections to the progression of human autoimmune diseases.

Md Al-Mustanjid, S M Hasan Mahmud, Farzana Akter, Md Shazzadur Rahman, Md Sajid Hossen, Md Habibur Rahman, Mohammad Ali Moni

Open access · goldAbstract read
In one paragraph

Article in Informatics in medicine unlocked, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 4 institutions in 1 country.

Md Al-MustanjidDepartment of Software Engineering, Faculty of Science and Information Technology, Daffodil International University, Dhaka-1207, Bangladesh.
S M Hasan MahmudDepartment of Computer Science, American International University-Bangladesh, Dhaka, 1229, Bangladesh.
Farzana AkterDepartment of Software Engineering, Faculty of Science and Information Technology, Daffodil International University, Dhaka-1207, Bangladesh.
Md Shazzadur RahmanDepartment of Computer Science & Engineering, Faculty of Science and Information Technology, Daffodil International University, Dhaka-1207, Bangladesh.
Md Sajid HossenDepartment of Software Engineering, Faculty of Science and Information Technology, Daffodil International University, Dhaka-1207, Bangladesh.
Md Habibur RahmanDepartment of Computer Science and Engineering, Islamic University, Kushtia-7003, Bangladesh.
Mohammad Ali MoniDepartment of Computer Science and Engineering, Pabna Science & Technology University, Pabna, 6600, Bangladesh.
Daffodil International University · BDAmerican International University-Bangladesh · BDIslamic University · BDPabna University of Science and Technology · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been circulating since 2019, and its global dominance is rising. Evidences suggest the respiratory illness SARS-CoV-2 has a sensitive affect on causing organ damage and other complications to the patients with autoimmune diseases (AD), posing a significant risk factor. The genetic interrelationships and molecular appearances between SARS-CoV-2 and AD are yet unknown. We carried out the transcriptomic analytical framework to delve into the SARS-CoV-2 impacts on AD progression. We analyzed both gene expression microarray and RNA-Seq datasets from SARS-CoV-2 and AD affected tissues. With neighborhood-based benchmarks and multilevel network topology, we obtained dysfunctional signaling and ontological pathways, gene disease (diseasesome) association network and protein-protein interaction network (PPIN), uncovered essential shared infection recurrence connectivities with biological insights underlying between SARS-CoV-2 and AD. We found a total of 77, 21, 9, 54 common DEGs for SARS-CoV-2 and inflammatory bowel disorder (IBD), SARS-CoV-2 and rheumatoid arthritis (RA), SARS-CoV-2 and systemic lupus erythematosus (SLE) and SARS-CoV-2 and type 1 diabetes (T1D). The enclosure of these common DEGs with bimolecular networks revealed 10 hub proteins (FYN, VEGFA, CTNNB1, KDR, STAT1, B2M, CD3G, ITGAV, TGFB3). Drugs such as amlodipine besylate, vorinostat, methylprednisolone, and disulfiram have been identified as a common ground between SARS-CoV-2 and AD from drug repurposing investigation which will stimulate the optimal selection of medications in the battle against this ongoing pandemic triggered by COVID-19.

Indexed as

Autoimmune diseasesCOVID-19DEGsDrug repurposingHub geneProtein-protein interaction network (PPIN)SARS-CoV-2Transcriptomic analysis

Identifiers

PMID35818398
PMCPMC9259025
OpenAlexW4285078354

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.