ArticleVirology journal2021
Human rhinovirus serotypes induces different immune responses.
Article in Virology journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The role of virus in nasal inflammation.European journal of medical research · 2025Review
- Creation of a Novel Coding Program to Identify Genes Controlled by miRNAs During Human Rhinovirus Infection.Methods and protocols · 2025Article
- SLC27A2 marks lipid peroxidation in nasal epithelial cells driven by type 2 inflammation in chronic rhinosinusitis with nasal polyps.Experimental & molecular medicine · 2025Article
- Human rhinovirus 16 induces an ICAM-1-PKR-ATF2 axis to modulate macrophage functions.Journal of virology · 2024Article
- Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions.Frontiers in allergy · 2024Review
- Different Clinical Presentations of Human Rhinovirus Species Infection in Children and Adults in Mexico.Open forum infectious diseases · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDifferent species of human rhinovirus (HRV) can induce varied antiviral and inflammatory responses in human blood macrophages and lower airway epithelium. Although human nasal epithelial cells (HNECs) are a primary infection route of HRV, differences between major and minor groups of HRV in the upper airway epithelium have not been studied in detail. In this study, we investigated viral replications and immune responses of major and minor groups of HRV in the HNECs.
methodsViral replication, immune responses of IFN-β, IFN-λ, proinflammatory cytokines, and viral receptors, and mRNA expression of transcription factors of HRV16 (major group) and HRV1B (minor group) in the HNECs were assessed.
resultsCompared with HRV16, HRV1B replicated more actively without excessive cell death and produced higher IFN-β, IFN-λ1/3, CXCL10, IL-6, IL-8, and IL-18 levels. Furthermore, low-density lipoprotein receptor (LDLR), TLR3, MDA5, NF-κB, STAT1, and STAT2 mRNA levels increased in HRV1B-infected HNECs.
conclusionHRV1B induces a stronger antiviral and inflammatory response from cell entry to downstream signaling compared with HRV16.
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Registered trials
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.