{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/86767"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/86767","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Characterization of the grvA and grvB Anti -Virulence Genes Encoded by the Gifsy-2 and Gifsy -1 Bacteriophages of Salmonella Typhimurium","abstract":"Salmonella enterica serovars cause diseases ranging from a mild, self-limiting gastroenteritis to a potentially life-threatening enteric fever in a variety of hosts. The serovar S. typhimurium causes a typhoid-like fever in mice which serves as an animal model of enteric fever. The lambdoid phages, Gifsy-1 and Gifsy-2, contribute significantly to S. typhimurium virulence. We have been studying biology of these phage to determine the effects of Gifsy-1 and Gifsy-2 on the virulence of S. typhimurium. The Gifsy-2 phage carries the periplasmic superoxide dismutase gene, sodCI. Using the IVET system, we identified a Salmonella specific gene grvA, a single open reading frame inserted in the opposite orientation in the tail operon of the Gifsy-2 phage. Contrary to classic virulence gene phenotypes, null mutants of grvA are more virulent than wild type when intraperitoneally inoculated into mice in competition assays. The grvA+ gene on a multi-copy plasmid also confers the anti-virulence phenotype. The anti-virulence phenotype conferred by the grvA null mutation and the grvA+ plasmid requires wild type sodCI. We have found that a second anti-virulence gene, grvB, located on the Gifsy-1 phage is also included in the GrvA-SodCI virulence cascade. Competition assays with null and over-expressing mutants show that the grvB gene confers anti-virulence phenotypes similar to that of grvA. The effects of grvB on virulence are also dependent upon the presence of wild type sodCI. These results suggest that GrvA and GrvB interact in the same virulence pathway to affect virulence in a SodCI dependent manner. Thus, in a wild type situation, GrvA and GrvB decrease the pathogenicity of S. typhimurium in the host, possibly by affecting resistance to toxic oxygen species.","abstract_html":"Salmonella enterica serovars cause diseases ranging from a mild, self-limiting gastroenteritis to a potentially life-threatening enteric fever in a variety of hosts. The serovar S. typhimurium causes a typhoid-like fever in mice which serves as an animal model of enteric fever. The lambdoid phages, Gifsy-1 and Gifsy-2, contribute significantly to S. typhimurium virulence. We have been studying biology of these phage to determine the effects of Gifsy-1 and Gifsy-2 on the virulence of S. typhimurium. The Gifsy-2 phage carries the periplasmic superoxide dismutase gene, sodCI. Using the IVET system, we identified a Salmonella specific gene grvA, a single open reading frame inserted in the opposite orientation in the tail operon of the Gifsy-2 phage. Contrary to classic virulence gene phenotypes, null mutants of grvA are more virulent than wild type when intraperitoneally inoculated into mice in competition assays. The grvA+ gene on a multi-copy plasmid also confers the anti-virulence phenotype. The anti-virulence phenotype conferred by the grvA null mutation and the grvA+ plasmid requires wild type sodCI. We have found that a second anti-virulence gene, grvB, located on the Gifsy-1 phage is also included in the GrvA-SodCI virulence cascade. Competition assays with null and over-expressing mutants show that the grvB gene confers anti-virulence phenotypes similar to that of grvA. The effects of grvB on virulence are also dependent upon the presence of wild type sodCI. These results suggest that GrvA and GrvB interact in the same virulence pathway to affect virulence in a SodCI dependent manner. Thus, in a wild type situation, GrvA and GrvB decrease the pathogenicity of S. typhimurium in the host, possibly by affecting resistance to toxic oxygen species.","abstract_has_math":false,"creators":["Ho, Theresa Deland"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Microbiology","degree_department":null,"school":null,"contributors":["Slauch, James M."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T15:17:56Z","date_published":"2015-09-28T15:17:56Z","updated_at":"2026-07-22T22:26:27Z","subjects":["Biology, Microbiology"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI9996638"],"render_values":[{"text":"(MiAaPQ)AAI9996638","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/86767","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Slauch, James M."]},{"key":"dc:creator","label":"Author","values":["Ho, Theresa Deland"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T15:17:56Z","10000-01-01","2001"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Microbiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Microbiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/86767","(MiAaPQ)AAI9996638"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Salmonella enterica serovars cause diseases ranging from a mild, self-limiting gastroenteritis to a potentially life-threatening enteric fever in a variety of hosts. The serovar S. typhimurium causes a typhoid-like fever in mice which serves as an animal model of enteric fever. The lambdoid phages, Gifsy-1 and Gifsy-2, contribute significantly to S. typhimurium virulence. We have been studying biology of these phage to determine the effects of Gifsy-1 and Gifsy-2 on the virulence of S. typhimurium. The Gifsy-2 phage carries the periplasmic superoxide dismutase gene, sodCI. Using the IVET system, we identified a Salmonella specific gene grvA, a single open reading frame inserted in the opposite orientation in the tail operon of the Gifsy-2 phage. Contrary to classic virulence gene phenotypes, null mutants of grvA are more virulent than wild type when intraperitoneally inoculated into mice in competition assays. The grvA+ gene on a multi-copy plasmid also confers the anti-virulence phenotype. The anti-virulence phenotype conferred by the grvA null mutation and the grvA+ plasmid requires wild type sodCI. We have found that a second anti-virulence gene, grvB, located on the Gifsy-1 phage is also included in the GrvA-SodCI virulence cascade. Competition assays with null and over-expressing mutants show that the grvB gene confers anti-virulence phenotypes similar to that of grvA. The effects of grvB on virulence are also dependent upon the presence of wild type sodCI. These results suggest that GrvA and GrvB interact in the same virulence pathway to affect virulence in a SodCI dependent manner. Thus, in a wild type situation, GrvA and GrvB decrease the pathogenicity of S. typhimurium in the host, possibly by affecting resistance to toxic oxygen species.","Made available in DSpace on 2015-09-28T15:17:56Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 9996638.pdf: 6925563 bytes, checksum: 4366ba16fed7f7d229d58d83a0526a1a (MD5) Previous issue date: 2001","Embargo set by: Seth Robbins for item 88048 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","171 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2001."]},{"key":"dc:title","label":"Title","values":["Characterization of the grvA and grvB Anti -Virulence Genes Encoded by the Gifsy-2 and Gifsy -1 Bacteriophages of Salmonella Typhimurium"]}]}],"canonical_facts":{"dc:contributor":["Slauch, James M."],"dc:creator":["Ho, Theresa Deland"],"dc:date":["2015-09-28T15:17:56Z","10000-01-01","2001"],"dc:description":["Salmonella enterica serovars cause diseases ranging from a mild, self-limiting gastroenteritis to a potentially life-threatening enteric fever in a variety of hosts. The serovar S. typhimurium causes a typhoid-like fever in mice which serves as an animal model of enteric fever. The lambdoid phages, Gifsy-1 and Gifsy-2, contribute significantly to S. typhimurium virulence. We have been studying biology of these phage to determine the effects of Gifsy-1 and Gifsy-2 on the virulence of S. typhimurium. The Gifsy-2 phage carries the periplasmic superoxide dismutase gene, sodCI. Using the IVET system, we identified a Salmonella specific gene grvA, a single open reading frame inserted in the opposite orientation in the tail operon of the Gifsy-2 phage. Contrary to classic virulence gene phenotypes, null mutants of grvA are more virulent than wild type when intraperitoneally inoculated into mice in competition assays. The grvA+ gene on a multi-copy plasmid also confers the anti-virulence phenotype. The anti-virulence phenotype conferred by the grvA null mutation and the grvA+ plasmid requires wild type sodCI. We have found that a second anti-virulence gene, grvB, located on the Gifsy-1 phage is also included in the GrvA-SodCI virulence cascade. Competition assays with null and over-expressing mutants show that the grvB gene confers anti-virulence phenotypes similar to that of grvA. The effects of grvB on virulence are also dependent upon the presence of wild type sodCI. These results suggest that GrvA and GrvB interact in the same virulence pathway to affect virulence in a SodCI dependent manner. Thus, in a wild type situation, GrvA and GrvB decrease the pathogenicity of S. typhimurium in the host, possibly by affecting resistance to toxic oxygen species.","Made available in DSpace on 2015-09-28T15:17:56Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 9996638.pdf: 6925563 bytes, checksum: 4366ba16fed7f7d229d58d83a0526a1a (MD5) Previous issue date: 2001","Embargo set by: Seth Robbins for item 88048 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","171 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2001."],"dc:identifier":["http://hdl.handle.net/2142/86767","(MiAaPQ)AAI9996638"],"dc:language":["eng"],"dc:subject":["Biology, Microbiology"],"dc:title":["Characterization of the grvA and grvB Anti -Virulence Genes Encoded by the Gifsy-2 and Gifsy -1 Bacteriophages of Salmonella Typhimurium"],"dc:type":["text"],"thesis:degree_discipline":["Microbiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:26:27Z"}