Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Variant rs4986790 of toll-like receptor 4 affects the signaling and induces cell dysfunction in patients with severe COVID-19.

International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases - 1 Jan 2024

Flores-Gonzalez Julio, Chavez-Galan Leslie, Falfán-Valencia Ramcés, Roldán Ivette Buendía, Fricke-Galindo Ingrid, Veronica-Aguilar Abigail, Martínez-Morales Alfonso, Hernández-Zenteno Rafael de Jesús, Guzmán-Guzmán Iris Paola, Pérez-Rubio Gloria

Abstract excerpt

OBJECTIVES: We investigated the expression of toll-like receptor (TLR)-4 on the cell surface of innate and adaptive cells from patients with COVID-19 carrying the rs4986790 GG genotype in the TLR4 gene and the functional profile of these cells. METHODS: We included 1169 hospitalized patients with COVID-19. The rs4986790 in TLR4 was identified by real-time polymerase chain reaction. Peripheral blood mononuclear...

Read the complete abstract on PubMed

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Topics

Share this publication in a Topic to start or enrich a Post.

Share to COVID-19
Share to Cytokines
Share to Genotype
Share to Leukocytes, Mononuclear
Share to Lipopolysaccharides
Share to SARS-CoV-2
Share to Severity of Illness Index
Share to Toll-Like Receptor 4

Source

Identifiers

PMID: 38029833
DOI: 10.1016/j.ijid.2023.11.032

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Variant rs4986790 of toll-like receptor 4 affects the signaling and induces cell dysfunction in patients with severe COVID-19.PMID 38029833Read ↗

TLR7 polymorphisms are associated with COVID-19 susceptibility and severity.Semantic proximity Read ↗

Toll-Like Receptor 4 Polymorphisms (896A/G and 1196C/T) as an Indicator of COVID-19 Severity in a Convenience Sample of Egyptian PatientsSemantic proximity Read ↗

Individual genetic variability mainly of Proinflammatory cytokines, cytokine receptors, and toll‐like receptors dictates pathophysiology of COVID‐19 diseaseSemantic proximity Read ↗

Innate Immune Gene Polymorphisms and COVID‐19 PrognosisSemantic proximity Read ↗

Innate Immune Gene Polymorphisms and COVID-19 PrognosisSemantic proximity Read ↗

Rare variants in Toll-like receptor 7 results in functional impairment and downregulation of cytokine-mediated signaling in COVID-19 patientsSemantic proximity Read ↗

COVID-19 susceptibility, severity, clinical outcome and Toll-like receptor (7) mRNA expression driven by TLR7 gene polymorphism (rs3853839) in middle-aged individuals without previous comorbiditiesSemantic proximity Read ↗

Variants rs3804099 and rs3804100 in the TLR2 Gene Induce Different Profiles of TLR-2 Expression and Cytokines in Response to Spike of SARS-CoV-2.Semantic proximity Read ↗

Implication of myddosome complex genetic variants in outcome severity of COVID-19 patients.Semantic proximity Read ↗

Prognostic impact of toll-like receptors gene polymorphism on outcome of COVID-19 pneumonia: A case-control study.Semantic proximity Read ↗

Interplay of TLR4 and SARS-CoV-2: Unveiling the Complex Mechanisms of Inflammation and Severity in COVID-19 InfectionsSemantic proximity Read ↗

Association of polymorphisms in TLR3 and TLR7 genes with susceptibility to COVID-19 among Iranian population: a retrospective case-control studySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.