A quantitative radioassay was used to study the factors affecting the adherence of 3H-labeled Staphylococcus aureus 1071 to Madin-Darby canine kidney cells, either uninfected or infected with the human FM1 strain of influenza A virus. Enhanced adherence to virus-infected cell cultures was independent of nonspecific factors-hydrophobicity, surface charge, and monolayer cell density. Viral hemagglutinin and neuraminidase did not act as the cell receptors for S. aureus because the growth of virus-inoculated monolayers in tunicamycin (an inhibitor of glycosylation) and the pretreatment of virus-infected cells with trypsin or virusspecific antiserum, which inhibit hemadsorption, had no effect on staphylococcal adherence. In contrast, adherence to uninfected and virus-infected cells was significantly reduced by protease treatment of either monolayers or staphylococci and by heat treatment of staphylococci. UV irradiation and treatment of bacteria with 0.1 M EDTA enhanced adherence. Pretreatment of monolayers with a thermal extract of S. aureus decreased adherence by 89 to 97%. The staphylococcal adhesin, which blocks adherence to virus-infected cells, appears to be a remarkably heat-stable, protease-and trypsin-sensitive macromolecule which is distinct from protein A, clumping factor, and teichoic acid. Lastly, pretreatment of S. aureus with human fibrinogen significantly enhanced adherence to virusinfected cells (P < 0.005) compared with binding with untreated S. aureus. The treated bacteria also adsorbed virus out of suspension. These results suggest that fibrinogen forms a bridge between S. aureus and receptors present on virusinfected cells and free virus.
