Table 1.

Pathogens for which NO• detoxification or repair has been identified as a virulence factor.

Pathogen	Gene(s)	Description	Ref.
E. coli (enterohemorrhagic)	norV	Strains harboring an inactive norV gene (norVs) exhibited reduced survival in murine macrophages.	[4]
E. coli (uropathogenic)	hmp	Isolates from patients with urinary tract infection had increased hmp expression, and Δhmp mutants were outcompeted by the wild-type in a mouse infection model.	[78]
M. tuberculosis	mpa, pafA uvrB, dlaT	Mutants deficient in proteasome components (mpa or pafA) [3] or nucleotide excision repair (uvrB) [31] exhibited attenuated virulence in mice.	[3,31]
N. meningitides	cycP, norB	Mutants lacking cytochrome c′ (cycP) or NO• reductase (norB) exhibited reduced survival in human macrophages and human nasopharyngeal mucosa organ cultures.	[6]
P. aeruginosa	norCBD	A mutant deficient in NO• reductase (norCBD) exhibited reduced viability in murine macrophages.	[8]
S. Typhimurium	hmp, xth, nfo, ytfE, STM1808	Mutants lacking hmp exhibited reduced survival in human macrophages [25] and attenuated virulence in mice [26]. Mutations in base excision repair (xth and nfo) [32], Fe-S assembly (ytfE) [7], or previously-unidentified STM1808 [7] each caused attenuated virulence in mice.	[7,25,26, 32]
S. aureus	hmp	Mutants deficient in hmp exhibited attenuated virulence in mice.	[79]
V. cholerae	hmpA	Mutants lacking hmpA were outcompeted in a mouse intestine colonization assay.	[5]
Y. pestis	hmp	A mutation in hmp resulted in longer incubation times and attenuated virulence in rats.	[30]