The role of the spv genes in Salmonella pathogenesis
- 1 Department of Medicine, University of California San Diego School of Medicine, La Jolla, CA, USA
- 2 Veterans Administration Medical Center, La Jolla, CA, USA
Salmonella strains cause three main types of diseases in people: gastroenteritis, enteric (typhoid) fever, and non-typhoid extra-intestinal disease with bacteremia. Genetic analysis indicates that each clinical syndrome requires distinct sets of virulence genes, and Salmonella isolates differ in their constellation of virulence traits. The spv locus is strongly associated with strains that cause non-typhoid bacteremia, but are not present in typhoid strains. The spv region contains three genes required for the virulence phenotype in mice: the positive transcriptional regulator spvR and two structural genes spvB and spvC. SpvB and SpvC are translocated into the host cell by the Salmonella pathogenicity island-2 type-three secretion system. SpvB prevents actin polymerization by ADP-ribosylation of actin monomers, while SpvC has phosphothreonine lyase activity and has been shown to inhibit MAP kinase signaling. The exact mechanisms by which SpvB and SpvC act in concert to enhance virulence are still unclear. SpvB exhibits a cytotoxic effect on host cells and is required for delayed cell death by apoptosis following intracellular infection. Strains isolated from systemic infections of immune compromised patients, particularly HIV patients, usually carry the spv locus, strongly suggesting that CD4 T cells are required to control disease due to Salmonella that are spv positive. This association is not seen with typhoid fever, indicating that the pathogenesis and immunology of typhoid have fundamental differences from the syndrome of non-typhoid bacteremia.
Keywords: Salmonella, spv, virulence, non-typhoid bacteremia, apoptosis, ADP-ribosylation, phosphothreonine lyase, CD4
Citation: Guiney DG and Fierer J (2011) The role of the spv genes in Salmonella pathogenesis. Front. Microbio. 2:129. doi: 10.3389/fmicb.2011.00129
Received: 16 March 2011;
Accepted: 25 May 2011;
Published online: 14 June 2011.
Edited by:John S. Gunn, The Ohio State University, USA
Reviewed by:Corrie Detweiler, University of Colorado Boulder, USA
Andres Vazquez-Torres, University of Colorado Medical School, USA
Copyright: © 2011 Guiney and Fierer. This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.
*Correspondence: Donald G. Guiney, Department of Medicine 0640, University of California San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0640, USA. e-mail: firstname.lastname@example.org