Rhinoviruses infect the lower airways.

Rhinoviruses are the major cause of the common cold and a trigger of acute asthma exacerbations. Whether these exacerbations result from direct infection of the lower airway or from indirect mechanisms consequent on infection of the upper airway alone is currently unknown. Lower respiratory infection was investigated in vitro by exposing primary human bronchial epithelial cells to rhinoviruses and in vivo after experimental upper respiratory infection of human volunteers. Bronchial infection was confirmed by both approaches. Furthermore, rhinoviruses induced production of interleukin-6, -8, and -16 and RANTES and were cytotoxic to cultured respiratory epithelium. This evidence strongly supports a direct lower respiratory epithelial reaction as the initial event in the induction of rhinovirus-mediated asthma exacerbations. The frequency of infection and the nature of the inflammatory response observed are similar to those of the upper respiratory tract, suggesting that rhinovirus infections may be one of the most important causes of lower in addition to upper respiratory disease.

[1]  A. Zuckerman,et al.  Principles and practice of clinical virology , 1999 .

[2]  N. Papadopoulos,et al.  Rhinovirus identification by BglI digestion of picornavirus RT-PCR amplicons , 1999, Journal of Virological Methods.

[3]  M. Schroth,et al.  Rhinovirus replication causes RANTES production in primary bronchial epithelial cells. , 1999, American journal of respiratory cell and molecular biology.

[4]  N. Papadopoulos,et al.  Rhinoviruses replicate effectively at lower airway temperatures , 1999, Journal of medical virology.

[5]  S. Johnston,et al.  Rhinovirus Infection Induces Expression of Its Own Receptor Intercellular Adhesion Molecule 1 (ICAM-1) via Increased NF-κB-mediated Transcription* , 1999, The Journal of Biological Chemistry.

[6]  S. Johnston,et al.  RANTES, Macrophage-Inhibitory Protein 1α, and the Eosinophil Product Major Basic Protein Are Released into Upper Respiratory Secretions during Virus-Induced Asthma Exacerbations in Children , 1999, The Journal of infectious diseases.

[7]  N. Papadopoulos,et al.  The acute exacerbation of asthma: Pathogenesis , 1999 .

[8]  M. Grunstein,et al.  Mechanism of rhinovirus-induced changes in airway smooth muscle responsiveness. , 1998, The Journal of clinical investigation.

[9]  S. Johnston,et al.  Low grade rhinovirus infection induces a prolonged release of IL-8 in pulmonary epithelium. , 1998, Journal of immunology.

[10]  W. Busse,et al.  Virus-induced airway hyperresponsiveness and asthma. , 1998, American journal of respiratory and critical care medicine.

[11]  G. Fine,et al.  Identification of IL-16 as the lymphocyte chemotactic activity in the bronchoalveolar lavage fluid of histamine-challenged asthmatic patients. , 1998, The Journal of allergy and clinical immunology.

[12]  R. Garofalo,et al.  Cell-Specific Expression of RANTES, MCP-1, and MIP-1α by Lower Airway Epithelial Cells and Eosinophils Infected with Respiratory Syncytial Virus , 1998, Journal of Virology.

[13]  I. van Ark,et al.  Involvement of IL-16 in the induction of airway hyper-responsiveness and up-regulation of IgE in a murine model of allergic asthma. , 1998, Journal of immunology.

[14]  M. Mäkelä,et al.  Viruses and Bacteria in the Etiology of the Common Cold , 1998, Journal of Clinical Microbiology.

[15]  M. Adachi,et al.  Expression of RANTES by normal airway epithelial cells after influenza virus A infection. , 1998, American journal of respiratory cell and molecular biology.

[16]  R. Garofalo,et al.  Cell-specific expression of RANTES, MCP-1, and MIP-1alpha by lower airway epithelial cells and eosinophils infected with respiratory syncytial virus. , 1998, Journal of virology.

[17]  K. Nakayama,et al.  Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1beta. , 1997, The American journal of physiology.

[18]  M. Yamaya,et al.  Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1β. , 1997, American journal of physiology. Lung cellular and molecular physiology.

[19]  M. Adachi,et al.  Expression of cytokines on human bronchial epithelial cells induced by influenza virus A. , 1997, International archives of allergy and immunology.

[20]  W. Busse,et al.  Detection of rhinovirus RNA in lower airway cells during experimentally induced infection. , 1997, American journal of respiratory and critical care medicine.

[21]  S. Johnston,et al.  Rhinoviruses induce interleukin-8 mRNA and protein production in human monocytes. , 1997, The Journal of infectious diseases.

[22]  W. Busse,et al.  The role of respiratory viruses in asthma. , 1997, Ciba Foundation symposium.

[23]  R. Garofalo,et al.  Transcriptional activation of the interleukin-8 gene by respiratory syncytial virus infection in alveolar epithelial cells: nuclear translocation of the RelA transcription factor as a mechanism producing airway mucosal inflammation , 1996, Journal of virology.

[24]  V. Hammersley,et al.  Risk factors for lower respiratory complications of rhinovirus infections in elderly people living in the community: prospective cohort study , 1996, BMJ.

[25]  S. Holgate,et al.  Experimental rhinovirus infection in volunteers. , 1996, The European respiratory journal.

[26]  V. Hammersley,et al.  Effects of upper respiratory tract infections in patients with cystic fibrosis. , 1996, Thorax.

[27]  M J Campbell,et al.  The relationship between upper respiratory infections and hospital admissions for asthma: a time-trend analysis. , 1996, American journal of respiratory and critical care medicine.

[28]  D. Proud,et al.  Infection of a human respiratory epithelial cell line with rhinovirus. Induction of cytokine release and modulation of susceptibility to infection by cytokine exposure. , 1995, The Journal of clinical investigation.

[29]  Stephen T Holgate,et al.  Community study of role of viral infections in exacerbations of asthma in 9-11 year old children , 1995, BMJ.

[30]  F. Hayden,et al.  Localization of human rhinovirus replication in the upper respiratory tract by in situ hybridization. , 1995, The Journal of infectious diseases.

[31]  S. Johnston,et al.  Lower airways inflammation during rhinovirus colds in normal and in asthmatic subjects. , 1995, American journal of respiratory and critical care medicine.

[32]  S. Johnston,et al.  Immunohistochemical analysis of nasal biopsies during rhinovirus experimental colds. , 1994, American journal of respiratory and critical care medicine.

[33]  S. Johnston,et al.  Detection of rhinovirus infection of the nasal mucosa by oligonucleotide in situ hybridization. , 1994, American journal of respiratory cell and molecular biology.

[34]  K. Nicholson,et al.  Respiratory viruses and exacerbations of asthma in adults. , 1993, BMJ.

[35]  S. Johnston,et al.  Use of polymerase chain reaction for diagnosis of picornavirus infection in subjects with and without respiratory symptoms , 1993, Journal of clinical microbiology.

[36]  A. Choi,et al.  Influenza virus A infection induces interleukin‐8 gene expression in human airway epitheial cells , 1992 .

[37]  A. Choi,et al.  Influenza virus A infection induces interleukin-8 gene expression in human airway epithelial cells. , 1992, FEBS letters.

[38]  R. Davies,et al.  Human nasal and bronchial epithelial cells in culture: an overview of their characteristics and function. , 1991, Allergy proceedings : the official journal of regional and state allergy societies.

[39]  J. Hendley,et al.  Respiratory virus infection of monolayer cultures of human nasal epithelial cells. , 1990, The American review of respiratory disease.

[40]  E. Lennette,et al.  Diagnostic Procedures for Viral, Rickettsial and Chlamydial Infections , 1989 .

[41]  A. Mcclelland,et al.  The major human rhinovirus receptor is ICAM-1 , 1989, Cell.

[42]  Elliot,et al.  Rhinovirus upper respiratory infection increases airway hyperreactivity and late asthmatic reactions. , 1989, The Journal of clinical investigation.

[43]  R. Turner,et al.  Histopathologic examination and enumeration of polymorphonuclear leukocytes in the nasal mucosa during experimental rhinovirus colds. , 1984, Acta oto-laryngologica. Supplementum.

[44]  P. Suratt,et al.  Pathogenesis of lower respiratory tract symptoms in experimental rhinovirus infection. , 1983, The American review of respiratory disease.

[45]  V. Swanson,et al.  Sudden death of an infant with rhinovirus infection complicating bronchial asthma: case report. , 1983, Pediatric pathology.

[46]  J. Hendley,et al.  Shedding of infected ciliated epithelial cells in rhinovirus colds. , 1982, The Journal of infectious diseases.

[47]  S. Reed,et al.  Role of viruses and bacteria in acute wheezy bronchitis in childhood: a study of sputum. , 1979, Archives of disease in childhood.

[48]  R. A. Killington,et al.  The effect of temperature on the synthesis of rhinovirus type 2 RNA. , 1977, The Journal of general virology.

[49]  G. Jackson,et al.  Transmission of the common cold to volunteers under controlled conditions. III. The effect of chilling of the subjects upon susceptibility. , 1958, American journal of hygiene.

[50]  G. Jackson,et al.  Transmission of the common cold to volunteers under controlled conditions. I. The common cold as a clinical entity. , 1958, A.M.A. archives of internal medicine.