Evidence map›Paper›PMID 33973174›Full record

ArticleAdvances in experimental medicine and biology2021

Coronavirus: Pure Infectious Disease or Genetic Predisposition.

Farzaneh Darbeheshti, Hassan Abolhassani, Mohammad Bashashati, Saeid Ghavami, Sepideh Shahkarami, Samaneh Zoghi, Sudhir Gupta, Jordan S Orange, Hans D Ochs, Nima Rezaei

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Article in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. 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

10 authors at 9 institutions in 8 countries.

Farzaneh DarbeheshtiDepartment of Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Hassan AbolhassaniDivision of Clinical Immunology, Department of Laboratory Medicine, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden.
Mohammad BashashatiDivision of Gastroenterology, Department of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA.
Saeid GhavamiDepartment of Human Anatomy and Cell Science, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Sepideh ShahkaramiMedical Genetics Network (MeGeNe), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Samaneh ZoghiResearch Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
Sudhir GuptaDepartment of Medicine, Division of Basic and Clinical Immunology, University of California, Irvine, CA, USA.
Jordan S OrangeImmunology, Allergy, and Rheumatology, Baylor College of Medicine and the Texas Children's Hospital, Houston, TX, USA.
Hans D OchsSchool of Medicine, Department of Pediatrics, University of Washington, Seattle, WA, USA.
Nima RezaeiResearch Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. rezaei_nima@tums.ac.ir.ORCID https://orcid.org/0000-0002-3836-1827
Universal Scientific Education and Research Network · IRAkademia Śląska · PLBaylor College of Medicine · USChildren's Medical Center · IREducation and Research Network · INKarolinska University Hospital · SETexas Tech University · USUniversity of California, Irvine · USUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes novel coronavirus disease (COVID-19), is the seventh pathogenic coronavirus recently discovered in December 2019 in Wuhan, China. To date, our knowledge about its effect on the human host remains limited. It is well known that host genetic factors account for the individual differences in the susceptibility to infectious diseases. The genetic susceptibility factors to COVID-19 and its severity are associated with several unanswered questions. However, the experience gained from an earlier strain of coronavirus, SARS-CoV-1, which shows 78% genetic similarity to SARS-CoV-2 and uses the same receptor to bind to host cells, could provide some clues. It, therefore, seems possible to assemble new evidence in order to solve a potential genetic predisposition puzzle for COVID-19. In this chapter, the puzzle pieces, including virus entry receptors, immune response, and inflammation-related genes, as well as the probable genetic predisposition models to COVID-19, are discussed.

Indexed as

Communicable DiseasesCOVID-19ChinaGenetic Predisposition to DiseaseHumansSARS-CoV-2COVID-19Genetic predispositionGenetic susceptibilityPolymorphismSARS-CoV-1SARS-CoV-2

Identifiers

PMID33973174
OpenAlexW3160594360

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.