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Journal of Virology, February 2002, p. 1109-1123, Vol. 76, No. 3
0022-538X/01/$04.00+0     DOI: 10.1128/JVI.76.3.1109-1123.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

VLA-2 ({alpha}2ß1) Integrin Promotes Rotavirus Entry into Cells but Is Not Necessary for Rotavirus Attachment

Max Ciarlet,1* Sue E. Crawford,1 Elly Cheng,1 Sarah E. Blutt,1 Daren A. Rice,1 Jeffrey M. Bergelson,2 and Mary K. Estes1

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030,1 Division of Immunologic and Infectious Diseases, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 191042

Received 27 July 2001/ Accepted 23 October 2001

In an attempt to identify the rotavirus receptor, we tested 46 cell lines of different species and tissue origins for susceptibility to infection by three N-acetyl-neuraminic (sialic) acid (SA)-dependent and five SA-independent rotavirus strains. Susceptibility to SA-dependent or SA-independent rotavirus infection varied depending on the cell line tested and the multiplicity of infection (MOI) used. Cells of renal or intestinal origin and transformed cell lines derived from breast, stomach, bone, or lung were all susceptible to rotavirus infection, indicating a wider host tissue range than previously appreciated. Chinese hamster ovary (CHO), baby hamster kidney (BHK-21), guinea pig colon (GPC-16), rat small intestine (Rie1), and mouse duodenum (MODE-K) cells were found to support only limited rotavirus replication even at MOIs of 100 or 500, but delivery of rotavirus particles into the cytoplasm by lipofection resulted in efficient rotavirus replication. The rotavirus cell attachment protein, the outer capsid spike protein VP4, contains the sequence GDE(A) recognized by the VLA-2 ({alpha}2ß1) integrin, and to test if VLA-2 is involved in rotavirus attachment and entry, we measured infection in CHO cells that lack VLA-2 and CHO cells transfected with the human {alpha}2 subunit (CHO{alpha}2) or with both the human {alpha}2 and ß1 subunits (CHO{alpha}2ß1) of VLA-2. Infection by SA-dependent or SA-independent rotavirus strains was 2- to 10-fold more productive in VLA-2-expressing CHO cells than in parental CHO cells, and the increased susceptibility to infection was blocked with anti-VLA-2 antibody. However, the levels of binding of rotavirus to CHO, CHO{alpha}2, and CHO{alpha}2ß1 cells were equivalent and were not increased over binding to susceptible monkey kidney (MA104) cells or human colonic adenocarcinoma (Caco-2, HT-29, and T-84) cells, and binding was not blocked by antibody to the human {alpha}2 subunit. Although the VLA-2 integrin promotes rotavirus infection in CHO cells, it is clear that the VLA-2 integrin alone is not responsible for rotavirus cell attachment and entry. Therefore, VLA-2 is not involved in the initial attachment of rotavirus to cells but may play a role at a postattachment level.

* Corresponding author. Mailing address: Department of Molecular Virology & Microbiology, Baylor College of Medicine, One Baylor Plaza, Mailstop BCM-385, Houston, TX 77030. Phone: (713) 798-4445. Fax: (713) 798-3586. E-mail: mciarlet{at}bcm.tmc.edu.

Journal of Virology, February 2002, p. 1109-1123, Vol. 76, No. 3
0022-538X/01/$04.00+0     DOI: 10.1128/JVI.76.3.1109-1123.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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