Abstract 1604 Poster Session II, Sunday, 5/2 (poster 102)

Many strains of Group B streptococci (GBS) express immunogenic surface proteins. The best characterized of these are the C proteins which are present in most non-Type III strains. The gene for the alpha C protein (bca) in prototype Ia/C strain A909 includes a series of nine tandem repeats of 246 bp which are identical at the nucleotide level. Analysis of clinical isolates of GBS reveals that the repeat number in bca is variable, ranging from 4-16 repeats. Deletion of tandem repeats occurs both in passage from human mother to neonate and in an immune mouse model. These findings suggest that antigenic variation at the level of repeat number in the alpha C protein may function as a means of escape from antibody-mediated host immunity. The mechanism by which excision of tandem repeat units in the bca gene is accomplished in vivo is unknown. The protein primarily responsible for recombination in bacteria is rec A, and we hypothesize that rec A-mediated homologous recombination facilities tandem repeat deletion and thus encodes a pathogenicity trait for GBS. To address the role of rec A in bca processing, we cloned the rec A gene from GBS. A 320 bp portion of the rec A gene was amplified from GBS genomic DNA using PCR primers designed by comparing conserved regions from other bacterial rec A genes. We constructed a cosmid library using strain A909 genomic DNA and used the rec A PCR product to identify the full GBS rec A sequence. At the amino acid level, this sequence is 52% identical to the E. coli rec A sequence. We are using the rec A sequence to construct rec A mutants and will compare bca processing in wild-type and rec A mutant GBS strains.