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Infection and Immunity, February 2000, p. 744-751, Vol. 68, No. 2
Department of Microbiology and Immunology,
Medical College of Ohio, Toledo, Ohio
43613-5806,1 and Department of
Microbiology, University of Alabama Birmingham, Birmingham, Alabama
352942
Received 26 August 1999/Returned for modification 6 October
1999/Accepted 28 October 1999
Passage in human blood of group A streptococcal isolate 64p was
previously shown to result in the enhanced expression of M and
M-related proteins. Similarly, when this isolate was injected into mice
via an air sac model for skin infection, organisms recovered from the
spleens showed both increased expression of M and M-related proteins
and increased skin-invasive potential. We show that these phenotypic
changes were not solely the result of increased transcription of the
mRNAs encoding the M and M-related gene products. Rather, the altered
expression was associated with posttranslational modifications of the M
and M-related proteins that occur in this strain, based on the presence
or absence of another virulence protein, the streptococcal cysteine
protease SpeB. The phenotypic variability also correlates with colony
size variation. Large colonies selected by both regimens expressed more
hyaluronic acid, which may explain differences in colony morphology.
All large-colony variants were SpeB negative and expressed three
distinct immunoglobulin G (IgG)-binding proteins in the M and M-related
protein family. Small-colony variants were SpeB positive and bound
little IgG through their M and M-related proteins because these
proteins, although made, were degraded or altered in profile by the
SpeB protease. We conclude that passage in either human blood or a
mouse selects for a stable, phase-varied strain of group A streptococci
which is altered in many virulence properties.
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Absence of SpeB Production in Virulent Large
Capsular Forms of Group A Streptococcal Strain 64
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Medical College of Ohio, 3055 Arlington Ave., Toledo, OH 43613-5806. Phone: (419) 383-4336. Fax: (419) 383-3002. E-mail: Mboyle{at}mco.edu.
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