Respiratory Virus Infection of Monolayer Cultures of Human Nasal Epithelial Cells
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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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”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [321]
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).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [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.”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [321]
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The airway epithelium: soldier in the fight against respiratory viruses
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Rhinoviruses infect the lower airways
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- Authors
- Winther, B., Gwaltney, J. M., & Hendley, J. O.
- Affiliations
- University of Copenhagen (DK)
- ORCID
- Winther, Birgit
- Venue
- American Review of Respiratory Disease
- Publisher
- Oxford University Press (OUP)
- 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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