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Paul S. Hoffman

Researcher at University of Virginia

Publications -  97
Citations -  5186

Paul S. Hoffman is an academic researcher from University of Virginia. The author has contributed to research in topics: Legionella pneumophila & Gene. The author has an hindex of 40, co-authored 96 publications receiving 4815 citations. Previous affiliations of Paul S. Hoffman include GlaxoSmithKline & Dalhousie University.

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Metronidazole resistance in Helicobacter pylori is due to null mutations in a gene (rdxA) that encodes an oxygen‐insensitive NADPH nitroreductase

TL;DR: It is shown that MtzR results from loss of oxygen‐insensitive NADPH nitroreductase activity, and suggests that many rdxA (MtzR) mutations may have been selected by prior use of Mtz against other infections.
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Surface-associated hsp60 chaperonin of Legionella pneumophila mediates invasion in a HeLa cell model.

TL;DR: A role for surface-exposed Hsp60 in invasion of HeLa cells by L. pneumophila is established as well as a monospecific anti-OmpS serum that inhibited the association of both virulent and avirulent strains of L.neumophila to He La cells, suggesting that while both HSp60 and OmpS may mediate bacterial association to HeLa Cells, only virulent strains selectively displayed Hsp 60 on their surfaces.
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Antiparasitic drug nitazoxanide inhibits the pyruvate oxidoreductases of Helicobacter pylori, selected anaerobic bacteria and parasites, and Campylobacter jejuni

TL;DR: It is proposed that NTZ− intercepts PFOR at an early step in the formation of the lactyl-TPP transition intermediate, resulting in the reversal of pyruvate binding prior to decarboxylation and in coordination with proton transfer to NTZ.
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Essential Thioredoxin-Dependent Peroxiredoxin System from Helicobacter pylori: Genetic and Kinetic Characterization

TL;DR: Allelic replacement mutagenesis revealed ahpC to be essential, suggesting a critical role for AhpC in defending H. pylori against oxygen toxicity.
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The Helicobacter pylori chemotaxis receptor TlpB (HP0103) is required for pH taxis and for colonization of the gastric mucosa.

TL;DR: P pH taxis, like motility and urease activity, is essential for colonization and persistence in the gastric mucosa, and thus TlpB function might represent a novel target in the development of therapeutics that blind tactic behavior.