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Journal of Virology, October 2001, p. 9312-9319, Vol. 75, No. 19
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.19.9312-9319.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Viral Evolution toward Change in Receptor Usage: Adaptation of a Major Group Human Rhinovirus To Grow in ICAM-1-Negative Cells

Andrea Reischl, Manuela Reithmayer, Gabriele Winsauer, Rosita Moser, Irene Gösler, and Dieter Blaas*

Institute of Medical Biochemistry, University of Vienna, A-1030 Vienna, Austria

Received 23 February 2001/Accepted 22 June 2001

Major receptor group common cold virus HRV89 was adapted to grow in HEp-2 cells, which are permissive for minor group human rhinoviruses (HRVs) but which only marginally support growth of major-group viruses. After 32 blind passages in these cells, each alternating with boosts of the recovered virus in HeLa cells, HRV89 acquired the capacity to effectively replicate in HEp-2 cells, attaining virus titers comparable to those in HeLa cells although no cytopathic effect was observed. Several clones were isolated and shown to replicate in HeLa cells whose ICAM-1 was blocked with monoclonal antibody R6.5 and in COS-7 cells, which are devoid of ICAM-1. Blocking experiments with recombinant very-low-density lipoprotein receptor fragments and enzyme-linked immunosorbent assays indicated that the mutants bound a receptor different from that used by minor-group viruses. Determination of the genomic RNA sequence encoding the capsid protein region revealed no changes in amino acid residues at positions equivalent to those involved in the interaction of HRV14 or HRV16 with ICAM-1. One mutation was within the footprint of a very-low-density lipoprotein receptor fragment bound to minor-group virus HRV2. Since ICAM-1 not only functions as a vehicle for cell entry but has also a "catalytic" function in uncoating, the use of other receptors must have important consequences for the entry pathway and demonstrates the plasticity of these viruses.

* Corresponding author. Mailing address: Institute of Medical Biochemistry, University of Vienna, Vienna Biocenter (VBC), Dr. Bohr Gasse 9/3, A-1030 Vienna, Austria. Phone: 43 1 4277 61630. Fax: 43 1 4277 9616. E-mail: dieter.blaas{at}univie.ac.at.

Journal of Virology, October 2001, p. 9312-9319, Vol. 75, No. 19
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.19.9312-9319.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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