Rhinoviral infection and asthma: the detection and management of rhinoviruses by airway epithelial cells

Authors

  • L. C. Parker,

    Corresponding author
    1. Academic Unit of Respiratory Medicine, Department of Infection and Immunity, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, UK
    • Correspondence:

      Lisa Parker, Academic Unit of Respiratory Medicine, Department of Infection and Immunity, Faculty of Medicine, Dentistry and Health, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK.

      E-mail: l.c.parker@sheffield.ac.uk

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  • C. A. Stokes,

    1. Academic Unit of Respiratory Medicine, Department of Infection and Immunity, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, UK
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  • I. Sabroe

    1. Academic Unit of Respiratory Medicine, Department of Infection and Immunity, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, UK
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Summary

Human rhinoviruses (HRV) have been linked to the development of childhood asthma and recurrent acute asthma exacerbations throughout life, and contribute considerably to the healthcare and economic burden of this disease. However, the ability of HRV infections to trigger exacerbations, and the link between allergic status and HRV responsiveness, remains incompletely understood. Whilst the receptors on human airway cells that detect and are utilized by most HRV group A and B, but not C serotypes are known, how endosomal pattern recognition receptors (PRRs) detect HRV replication products that are generated within the cytoplasm remains somewhat of an enigma. In this article, we explore a role for autophagy, a cellular homeostatic process that allows the cell to encapsulate its own cytosolic constituents, as the crucial mechanism controlling this process and regulating the innate immune response of airway epithelial cells to viral infection. We will also briefly describe some of the recent insights into the immune responses of the airway to HRV, focusing on neutrophilic inflammation that is a potentially unwanted feature of the acute response to viral infection, and the roles of IL-1 and Pellinos in the regulation of responses to HRV.

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