Streptococcus agalactiae, also known as Group B Streptococcus
(GBS), is one of the most common causes of invasive infections
including sepsis, meningitis, and pneumonia in neonates and
immunocompromised patients. A major virulence factor
encoded by all nine serotypes of GBS is the surface protein, C5a
peptidase r (SCPB). This enzyme specifically degrades the human
C5a chemotaxin and promotes intracellular invasion of epithelial
cells. Previous experiments revealed that some clinical serotype
V strains contain a partial deletion within the scpB gene. This
study investigates whether these strains are a unique lineage
and are functionally similar to each other but different from
strains that lack the scpB deletion. I postulated that the strains
containing the deletion are clonally related and that the deletion
in scpB reduces the ability of strains to invade HEp2 cells. A western blot using antibodies against the SCPB protein was performed on both mutant and wild type strains in order to confirm the absence of SCPB in the mutant strains. Invasion assays were conducted on various serotype V strains and showed that the strains with the scpB deletion invaded at a similar rate in comparison to each other suggesting that these strains belong to the same lineage. The comparison of DNA fragments produced by restriction fragment length polymorphism (RFLP) on these mutant strains also supports this theory. However, contrary to my hypothesis, strains containing the deletion demonstrated a higher percent invasion versus the wild type strain. To further investigate this finding and the relatedness of these strains, an adherence assay will be performed to determine if there is a difference in the ability to adhere to epithelial cells between mutant and wild type strains.
Additional contributors: Sarah Briscoe; Aaron Gillman; Katelyn Reagan; Dileepan T; Beinan
Wang; Patricia Ferrieri; Patrick Cleary (faculty mentor).
Impact of a Genetic Deletion on the Capacity of Group B Strepococcus to Invade Human Epithelial Cells.
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