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Mouse respiratory epithelial cells support efficient replication of human rhinovirus

Nikolaos G. Papadopoulos^2,

Suzanne Barnard^4,

Edward D. Blair^4,

¹ Division of Microbiology, School of Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, UK
² University Medicine, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK
³ Department of Respiratory Medicine, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK
⁴ GlaxoSmithKline Medicines Research Centre, Stevenage SG1 2NY, UK

Correspondence
Tobias Tuthill
t.tuthill{at}bmb.leeds.ac.uk

Human rhinoviruses (HRV) are responsible for the majority of virus infections of the upper respiratory tract. Furthermore, HRV infection is associated with acute exacerbation of asthma and other chronic respiratory diseases of the lower respiratory tract. A small animal model of HRV-induced disease is required for the development of new therapies. However, existing mouse models of HRV infection are difficult to work with and until recently mouse cell lines were thought to be generally non-permissive for HRV replication in vitro. In this report we demonstrate that a virus of the minor receptor group, HRV1B, can infect and replicate in a mouse respiratory epithelial cell line (LA-4) more efficiently than in a mouse fibroblast cell line (L). The major receptor group virus HRV16 requires human intercellular adhesion molecule-1 (ICAM-1) for cell entry and therefore cannot infect LA-4 cells. However, transfection of in vitro-transcribed HRV16 RNA resulted in the replication of viral RNA and production of infectious virus. Expression of a chimeric ICAM-1 molecule, comprising mouse ICAM-1 with extracellular domains 1 and 2 replaced by the equivalent human domains, rendered the otherwise non-permissive mouse respiratory epithelial cell line susceptible to entry and efficient replication of HRV16. These observations suggest that the development of mouse models of respiratory tract infection by major as well as minor group HRV should be pursued.

Present address: Research Laboratories, 2nd Department of Pediatrics, University of Athens, 13 Levadias Street, 11527 Goudi, Athens, Greece.

Present address: Division of Virology, University of Glasgow, Church Street, Glasgow G11 5JR, UK.

Present address: Integrated Medicines Consulting Ltd, Topfield House, Ermine Street, Caxton, Cambridgeshire CB3 8PQ, UK.