Type 2 rhinovirus infection of cultured human tracheal epithelial cells: role of LDL receptor.

@article{Suzuki2001Type2R,
  title={Type 2 rhinovirus infection of cultured human tracheal epithelial cells: role of LDL receptor.},
  author={T. Suzuki and M. Yamaya and Masato Kamanaka and Y. X. Jia and Katsutoshi Nakayama and Masayoshi Hosoda and Norihiro Yamada and H. Nishimura and Kiyohisa Sekizawa and Hidetada Sasaki},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2001},
  volume={280 3},
  pages={
          L409-20
        }
}
  • T. Suzuki, M. Yamaya, +7 authors H. Sasaki
  • Published 1 March 2001
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
To examine the role of the low-density lipoprotein (LDL) receptor on minor group human rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with a minor group (RV2) or a major group (RV14) RV. Viral infection was confirmed by showing with PCR that viral titers in supernatants and lysates from infected cells increased with time. RV2 and RV14 increased expression of mRNA and protein of the LDL receptor on the cells and the cytokine production. RV2 induced… 
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Erythromycin inhibits rhinovirus infection in cultured human tracheal epithelial cells.
TLDR
The results suggest that erythromycin inhibits infection by the major RV subgroup by reducing ICAM-1 and infection by both RV subgroups by blocking the RV RNA entry into the endosomes.
Toll-Like Receptor 3 Is Induced by and Mediates Antiviral Activity against Rhinovirus Infection of Human Bronchial Epithelial Cells
TLDR
It is demonstrated that blocking TLR3 led to a decrease in interleukin-6, CXCL8, and CCL5 in response to poly(IC) but an increase following RV infection, and it was demonstrated thatTLR3 mediated the antiviral response.
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TLDR
This is the first report of genetically similar viruses eliciting dissimilar cytokine release, transcription factor phosphorylation, and MAPK activation from macrophages, suggesting that receptor use is a mechanism for establishing the inflammatory microenvironment in the human airway upon exposure to rhinovirus.
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TLDR
It is demonstrated that inhibiting Rac resulted in the upregulation of TLR3 in macrophages exposed to major- and minor-group HRV, and resulted in increased release of IFN-α, and suggest that Rac is an important regulator in establishing the inflammatory microenvironment that is initiated in the human airway upon exposure to rhinovirus.
Rhinovirus C replication is associated with the endoplasmic reticulum and triggers cytopathic effects in an in vitro model of human airway epithelium
TLDR
Describing RV-C15 replication at the single-cell level and its impact on the human airway epithelium using a physiologically-relevant in vitro model reveals that – unlike other RVs – the endoplasmic reticulum is the primary site for RV- C15 replication.
The role of the Ras superfamily small G-proteins in the proinflammatory environment of rhinovirus-exposed monocytic-lineage cells
TLDR
It is demonstrated that the small G-protein Rac is differentially activated when majorand minorgroup HRV bind to macrophage ICAM-1 or LDL receptors, which suggests that Rac is important in establishing the inflammatory microenvironment that is initiated in the human airway upon exposure to rhinovirus.
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TLDR
A coding single nucleotide polymorphism in CDHR3 could promote RV-C infections and illnesses in infancy, which could in turn adversely affect the developing lung to increase the risk of asthma.
Rhinovirus and asthma.
TLDR
The pathogenesis and management of RV infection-induced exacerbation of bronchial asthma is reviewed and soluble ICAM-1 and erythromycin were reported to reduce the frequency of common colds.
Attenuation of the type I interferon response in cells infected with human rhinovirus.
Clinical Importance of Rhinovirus Infection on COPD Exacerbation
TLDR
Macrolide antibiotics bafilomycin A1 and erythromycin inhibit RV infection by reducing the expression of ICAM-1, the major RVs receptor, and by blocking RV entry, which reduced the frequency of common colds and COPD exacerbations.
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