Cited by 124Respiratory viral infections researchViral Infections and Immunology ResearchInfluenza Virus Research Studies

Respiratory Virus Infection of Monolayer Cultures of Human Nasal Epithelial Cells

Winther, Birgit, Gwaltney, Jack M., Hendley, J. Owen·1990·American Review of Respiratory Disease

Abstract

The effect on nasal epithelial cells in monolayer cultures of infection with rhinovirus, coronavirus 229E, influenza type A, and adenovirus was studied. Fragments (1 × 2 mm) of epithelium with adherent submucosa from nasal polyps, adenoids, or nasal turbinates were cultured in plastic dishes with media containing a serum supplement. Within a week a monolayer of epithelial cells with interspersed ciliated cells surrounded each fragment. Epithelial monolayers were exposed to 103 to 104 TCID50/ml of each virus; unattached virus was removed after 3 h. Replication of virus was examined by doing viral titrations of the media daily, and ciliated and nonciliated epithelial cells in the monolayer were examined morphologically with an inverted microscope. The peak titer of rhinovirus and coronavirus occurred 24 to 48 h after inoculation, indicating that viral replication was occurring. However, no detectable damage or cytopathic effect (CPE) developed in the monolayer of epithelial cells when compared with that in uninfected control cells. In contrast, infection of epithelial monolayers with influenza or adenovirus resulted in CPE and destruction of the monolayer. The marked difference in the effect of these respiratory viruses on nasal epithelial cells may reflect similar differences in their effect on respiratory tract mucosa in the intact host. If so, the pathogenesis of symptom production during rhinovirus and coronavirus infections must be by mechanisms other than destruction of the nasal lining.

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Crossref · 10.1164/ajrccm/141.4_pt_1.839

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7 of 7 references verified0 citation errors · 0 not checkable

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  • Under an atopic environment, the epithelial inflammatory response to rhinoviruses is downregulated and associated with increased viral proliferation and augmented cell damage.

    “For instance, it has been shown that under the influence of an atopic environment, the epithelial inflammatory response to rhinoviruses is downregulated and associated with increased viral proliferation and augmented cell damage”
  • The downregulation of epithelial inflammatory response to rhinoviruses in an atopic environment suggests a potential mechanism to explain the propensity of atopic asthmatic individuals to develop lower airway symptoms after respiratory infections.

    “suggesting a potential mechanism to explain the propensity of atopic asthmatic individuals to develop lower airway symptoms after respiratory infections (321).”
  • The environment to which airway epithelial cells are exposed influences the inflammatory response to respiratory viruses.

    “Besides the virus type, the environment to which airway epithelial cells are exposed influences the inflammatory response to respiratory viruses.”

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Authors
Winther, B., Gwaltney, J. M., & Hendley, J. O.
Affiliations
University of Copenhagen (DK)
Venue
American Review of Respiratory Disease
Published
1990-04-01
Volume
141
Issue
4_Part_1
Pages
839-845
ISSN
0003-0805 (ISSN-L)
OpenAlex
W2048697537
Cited by
124
References
7
Citations by year
2025: 2 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 3 · 2019: 6 · 2018: 3 · 2017: 5 · 2016: 3 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 6
FWCI
3.36
Type
journal article
Language
en
Open access
closed
Locations
  • American Review of Respiratory Disease (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
Keywords
respiratory viruses, nasal epithelial cells, rhinovirus, HCoV-229E, adenovirus, viral replication, cytopathic effect, ciliated cells, nasal polyps, adenoids, viral pathogenesis, respiratory mucosa
MeSH terms
Adenoids, Adenoviridae Infections, Cells, Cultured, Coronaviridae Infections, Cytopathogenic Effect, Viral, Humans, Influenza, Human, Nasal Mucosa, Nasal Polyps, Picornaviridae Infections, Respiratory Tract Infections, Rhinovirus, Virus Diseases, Virus Replication

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