Evidence map›Paper›PMID 35062298›Full record

ReviewViruses2022

Implications of the Immune Polymorphisms of the Host and the Genetic Variability of SARS-CoV-2 in the Development of COVID-19.

Jesús Zepeda-Cervantes, Daniel Martínez-Flores, Josué Orlando Ramírez-Jarquín, Ángeles C Tecalco-Cruz, Noé Santiago Alavez-Pérez, Luis Vaca, Rosa Elena Sarmiento-Silva

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 14 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 3 institutions in 1 country.

Jesús Zepeda-CervantesDepartamento de Microbiología e Inmunología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Daniel Martínez-FloresDepartamento de Biología Celular y del Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0002-3769-4996
Josué Orlando Ramírez-JarquínDepartamento de Neuropatología Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Ángeles C Tecalco-CruzPosgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México (UACM), Mexico City 06720, Mexico.
Noé Santiago Alavez-PérezEscuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Mexico City 07340, Mexico.
Luis VacaDepartamento de Biología Celular y del Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0003-2266-4847
Rosa Elena Sarmiento-SilvaDepartamento de Microbiología e Inmunología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0001-7430-5657
Universidad Nacional Autónoma de México · MXInstituto Politécnico Nacional · MXUniversidad Autónoma de la Ciudad de México · MX

Funding

Dirección General de Asuntos del Personal Académico AV200320Dirección General de Asuntos del Personal Académico IN2222020
6 · The paper itself

Abstract

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the current pandemic affecting almost all countries in the world. SARS-CoV-2 is the agent responsible for coronavirus disease 19 (COVID-19), which has claimed millions of lives around the world. In most patients, SARS-CoV-2 infection does not cause clinical signs. However, some infected people develop symptoms, which include loss of smell or taste, fever, dry cough, headache, severe pneumonia, as well as coagulation disorders. The aim of this work is to report genetic factors of SARS-CoV-2 and host-associated to severe COVID-19, placing special emphasis on the viral entry and molecules of the immune system involved with viral infection. Besides this, we analyze SARS-CoV-2 variants and their structural characteristics related to the binding to polymorphic angiotensin-converting enzyme type 2 (ACE2). Additionally, we also review other polymorphisms as well as some epigenetic factors involved in the immunopathogenesis of COVID-19. These factors and viral variability could explain the increment of infection rate and/or in the development of severe COVID-19.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsAntigenic Drift and ShiftCOVID-19Genetic Predisposition to DiseaseGenetic VariationHost-Pathogen InteractionsHumansPolymorphism, GeneticSARS-CoV-2Angiotensin-Converting Enzyme 2ACE2 overexpressiongenetic susceptibilityimmune polymorphismSARS-CoV-2 variantsevere COVID-19

Identifiers

PMID35062298
PMCPMC8778858
OpenAlexW4206054462

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.