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The genome of the Philadelphia-1 strain ofLegionella pneumophila , the causative organism of Legionnaires' disease, encodes two virulence-associated type 4 secretion systems (T4SSs), the Dot/Icm type 4B (T4BSS) and the Lvh type 4A (T4ASS). Broth stationary-phase cultures of mostdot/icm mutants are defective in entry and evasion of phagosome acidification. However, those virulence defects can be reversed by incubating broth cultures ofdot/icm mutants in water, termed water stress (WS). WS reversal requires thelvh T4ASS locus, suggesting an interaction between the two T4SSs in producingLegionella virulence phenotypes. In the current work, the loss of WS reversal in adotA Δlvh mutant of strain JR32 was shown to be attributable to loss of thelvh virD4 gene, encoding the putative coupling protein of the T4ASS. Transformation of adotA Δlvh mutant withvirD4 also reversed entry and phagosome acidification defects in broth cultures. In addition, broth cultures of Δlvh and ΔvirD4 mutants, which weredot/icm + , showed 5-fold and &gt;6-fold increases in translocation of the Dot/Icm translocation substrates, proteins RalF and SidD, respectively. These data demonstrate that the Lvh T4ASS functions in both broth stationary-phase cultures conventionally used for infection and cultures exposed to WS treatment. Our studies in adotA Δlvh mutant and in adot/icm + background establish that VirD4 and the Lvh T4ASS contribute to virulence phenotypes and are consistent with independent functioning of Dot/Icm and Lvh T4SSs or functional substitution of the Lvh VirD4 protein for a component(s) of the Dot/Icm T4BSS.

Implication of the VirD4 Coupling Protein of the Lvh Type 4 Secretion System in Virulence Phenotypes of Legionella pneumophila