Abstract
Group A streptococci produce a number of suppurative infections in man including acute pharyngitis, impetigo, cellulitis, erysipelas and septicemia (Bisno, 1979a). Two sequelae, acute rheumatic fever or acute glomerulonephritis, may follow infection and may be related to hyper-immune responsiveness in the host (Bisno, 1979 b,c). A number of reports have suggested that the post-streptococcal sequelae are a result of molecular mimicry between streptococcal M proteins and α-helical coiled-coil proteins in the host tissues (Krisher and Cunningham, 1985; Dale and Beachey, 1985a, 1986; Manjula and Fischetti, 1986; Cunningham and Swerlick, 1986; Cunningham et al., 1989; Fenderson et al., 1989; Kraus et al., 1989). Streptococcal membrane proteins have also been implicated in the immunological crossreactions between streptococci and heart (Zabriskie and Freimer, 1966; van de Rijn et al 1977; Cunningham et al, 1984; Barnett and Cunningham, 1990).
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Cunningham, M.W. (1992). Group A Streptococci: Molecular Mimicry, Autoimmunity and Infection. In: Hook, M., Switalski, L. (eds) Microbial Adhesion and Invasion. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-2924-7_13
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DOI: https://doi.org/10.1007/978-1-4612-2924-7_13
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