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Journal of Virology, July 2004, p. 6974-6981, Vol. 78, No. 13
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.13.6974-6981.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The VP7 Outer Capsid Protein of Rotavirus Induces Polyclonal B-Cell Activation

Sarah E. Blutt,¹ Sue E. Crawford,¹ Kelly L. Warfield,^1, Dorothy E. Lewis,² Mary K. Estes,¹ and Margaret E. Conner^1,3*

Department of Molecular Virology and Microbiology,¹ Department of Immunology, Baylor College of Medicine ,² Medical Research Service, Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas 77030³

Received 31 October 2003/ Accepted 26 February 2004

The early response to a homologous rotavirus infection in mice includes a T-cell-independent increase in the number of activated B lymphocytes in the Peyer's patches. The mechanism of this activation has not been previously determined. Since rotavirus has a repetitively arranged triple-layered capsid and repetitively arranged antigens can induce activation of B cells, one or more of the capsid proteins could be responsible for the initial activation of B cells during infection. To address this question, we assessed the ability of rotavirus and virus-like particles to induce B-cell activation in vivo and in vitro. Using infectious rotavirus, inactivated rotavirus, noninfectious but replication-competent virus, and virus-like particles, we determined that neither infectivity nor RNA was necessary for B-cell activation but the presence of the rotavirus outer capsid protein, VP7, was sufficient for murine B-cell activation. Preincubation of the virus with neutralizing VP7 antibodies inhibited B-cell activation. Polymyxin B treatment and boiling of the virus preparation were performed, which ruled out possible lipopolysaccharide contamination as the source of activation and confirmed that the structural conformation of VP7 is important for B-cell activation. These findings indicate that the structure and conformation of the outer capsid protein, VP7, initiate intestinal B-cell activation during rotavirus infection.

Present address: Division of Toxinology and Aerobiology, United States Research Institute of Infectious Diseases, 1425 Porter St., Fort Detrick, MD 21702.

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