Factors Influencing Adherence of Staphylococcus aureus to Influenza A Virus-Infected Cell Cultures

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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 virus-specific 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 virus-infected 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 virus-infected cells and free virus.

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