Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 188, Issue 4, Pages 486-496Publisher
UNIV CHICAGO PRESS
DOI: 10.1086/377098
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Funding
- NIAID NIH HHS [5T32 AI07180-21] Funding Source: Medline
- NIDDK NIH HHS [R01 DK58587] Funding Source: Medline
- NIGMS NIH HHS [R01 GM63270] Funding Source: Medline
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The highly diverse bacterium Helicobacter pylori, which persistently colonizes the human stomach, provides models to study the role of genome plasticity in host adaptation. Within H. pylori populations from 2 colonized individuals, intragenomic recombination between cagA DNA repeat sequences leads to deletion or duplication of tyrosine phosphorylation sites in the CagA protein, which is injected by a type IV secretion system into host cells. Experimental coculture of gastric epithelial cells with the strains containing these naturally occurring CagA phosphorylation site variants induced markedly divergent host cell morphologic responses. Mutants were constructed in which a phosphorylation site was either added or deleted in the expressed CagA protein; coculture studies confirmed that the naturally occurring differences in CagA phosphorylation are responsible for the observed phenotypic variation. These findings indicate that within an individual host, intragenomic recombination between H. pylori repetitive DNA produces strain variants differing in their signals to host cells.
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