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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Updated: Oct 11, 2025

Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
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Human rhinovirus serotypes induces different immune responses.

Ji Heui Kim1, Jung Yeon Jang1, Yong Ju Jang2

  • 1Department of Otorhinolaryngology - Head and Neck Surgery, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Republic of Korea.

Virology Journal
|November 28, 2021
PubMed
Summary

Human rhinovirus 1B (HRV1B) triggers a more robust antiviral and inflammatory response in nasal cells than HRV16. This involves increased viral replication and heightened immune signaling pathways, impacting upper airway immunity.

Keywords:
CytokinesHuman rhinovirusIL-8InterferonMDA5NF-κBTLR3

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Area of Science:

  • Virology
  • Immunology
  • Respiratory Medicine

Background:

  • Human rhinoviruses (HRVs) are a major cause of respiratory infections.
  • While HRVs infect the upper airway, differences in immune responses between major and minor HRV groups in nasal epithelium are not well understood.

Purpose of the Study:

  • To compare viral replication and immune responses of major (HRV16) and minor (HRV1B) HRV groups in human nasal epithelial cells (HNECs).

Main Methods:

  • Assessed viral replication, interferon (IFN)-β, IFN-λ, pro-inflammatory cytokines, viral receptors, and transcription factor mRNA in HRV-infected HNECs.
  • Compared HRV16 (major group) and HRV1B (minor group) infections.

Main Results:

  • HRV1B replicated more actively than HRV16 with less cell death.
  • HRV1B induced higher levels of IFN-β, IFN-λ1/3, CXCL10, IL-6, IL-8, and IL-18.
  • Upregulation of LDLR, TLR3, MDA5, NF-κB, STAT1, and STAT2 mRNA was observed in HRV1B-infected HNECs.

Conclusions:

  • HRV1B elicits a stronger antiviral and inflammatory response in HNECs compared to HRV16.
  • This response involves enhanced viral entry, replication, and downstream immune signaling pathways.