FIG. 4.

MA104 cell treatment with high concentrations of DGEA does not induce cell surface expression of α2β1, β2, and αvβ3 integrins (A), but the loss of DGEA-mediated inhibition of SA11 infectivity is inhibited by genistein (B). (A) Flow cytometric histograms. Cells were treated with 2.0 mM DGEA, control peptide GHRP, or mock treated, and their surface integrin expression levels were determined by flow cytometry after staining with monoclonal antibodies AK7 (α2I), P4H9-A11 (β2), and LM609 (αvβ3). Cells were also stained with isotype control monoclonal antibody MOPC21 at the same concentration as each test monoclonal antibody (control). Mock-treated and peptide-treated cells stained with MOPC21 gave identical histograms (control). In panel B, cells were mock treated or treated with 10 μM genistein prior to incubation with peptide DGEA or GHRP at concentrations ranging from 0.015 to 1.0 mM, followed by assay of SA11 rotavirus infectivity, as described in Materials and Methods. The infectivity titer of SA11 in cells treated with peptide with and without genistein is expressed as a percentage of the titer obtained in the absence of peptide or genistein.