November 27, 2021Virology JournalOpen Access

Human rhinovirus serotypes induces different immune responses

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Why the study?

Differences between major and minor groups of human rhinovirus in upper airway epithelium have not been studied in detail, despite human nasal epithelial cells being a primary infection route.

Does HRV1B induce a different antiviral and inflammatory response compared to HRV16 in human nasal epithelial cells?

Structured PICO

Does HRV1B induce a different antiviral and inflammatory response compared to HRV16 in human nasal epithelial cells?

Population

Human nasal epithelial cells (HNECs) obtained from the middle turbinate of 8 healthy subjects (4 males, 4 females, ages 19-49) undergoing septoplasty, with no history of allergy, asthma, upper respiratory infection, or recent corticosteroid/antibiotic use.

Intervention

Infection with human rhinovirus 1B (HRV1B, minor group) at a multiplicity of infection (MOI) of 0.5 for 72 hours.

Comparator

Infection with human rhinovirus 16 (HRV16, major group) at MOI 0.5, and mock-infection with phosphate buffered saline (PBS).

Outcome

Viral replication and immune responses including production of IFN-β, IFN-λ, proinflammatory cytokines, and mRNA expression of viral receptors and transcription factors at 72 hours post-infection.surrogate

The minor group rhinovirus HRV1B induces a stronger antiviral and inflammatory response in human nasal epithelial cells compared to the major group HRV16.

Limitations

Results may not be broadly applied to other serotypes in HRV-A-major and -minor groups.
Discrepancies with other studies may be due to differences in cell source, viral load, and location of sample collection.

Implication

Minor-group HRV may drive stronger nasal epithelial responses than major-group; leaves open in vivo relevance and clinical translation.

Abstract

BACKGROUND: Different 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. METHODS: Viral 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. RESULTS: Compared 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. CONCLUSION: HRV1B induces a stronger antiviral and inflammatory response from cell entry to downstream signaling compared with HRV16.