Infection and Immunity, December 2000, p. 7132-7136, Vol. 68, No. 12
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Copyright © 2000, American Society for Microbiology. All rights reserved.

SIGA Research Laboratories, Corvallis, Oregon 973331; Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, New York 100212; and Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 731903
Received 1 March 2000/Returned for modification 14 June 2000/Accepted 18 September 2000
Archived sera (collected in 1946) from acute rheumatic fever (ARF) and untreated scarlet fever and/or pharyngitis patients were reacted with streptococcal M protein, cardiac myosin, and cardiac tropomyosin. Except for very low levels to tropomyosin, antibodies to other antigens were not elevated in the sera of ARF patients relative to those of non-ARF patients, even though there was roughly equivalent exposure to group A streptococci. This suggests that antibodies to these molecules may not play a central role in the induction of ARF.
Present address: LID, NIAID, National Institutes of Health,
Bethesda, MD 20892-0720.
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