Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 200, Issue 5, Pages 724-734Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/604728
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Funding
- Intramural research program of the National Institute of Allergy and Infectious Diseases
- National Institutes of Health
- Departments of Pediatrics and Microbiology, University of Chicago
- [RN6390]
- [LUG776]
- [LUG855]
- [LUG862]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001079, ZIAAI000904] Funding Source: NIH RePORTER
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sThe role of Panton-Valentine leukocidin (PVL) in Staphylococcus aureus pathogenesis is controversial. Here, we show that an unintended point mutation in the agr P2 promoter of S. aureus caused the phenotypes in gene regulation and murine pneumonia attributed to PVL by earlier investigators. In agreement with other studies that failed to detect similar effects of PVL using community-associated methicillin-resistant S. aureus strains, we found no significant effect of PVL on gene expression or pathogenesis after we repaired the mutation. These findings provide further evidence that PVL does not have a major impact on S. aureus pathogenesis. Moreover, our results demonstrate that a single nucleotide polymorphism in an intergenic region can dramatically affect bacterial physiology and virulence. Finally, our work emphasizes the need to frequently evaluate the integrity of the S. aureus agr locus.
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