ArticlemBio2015
Targeted knockout of the Rickettsia rickettsii OmpA surface antigen does not diminish virulence in a mammalian model system.
Article in mBio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 78 citations in OpenAlex.
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- VapC toxins promote the pathogenesis of Rickettsia heilongjiangensis by cleaving essential RNAs from both Rickettsia and its host.PLoS pathogens · 2025Article
- Phosphatidylserine-binding receptor, CD300f, on macrophages mediates host invasion of pathogenic and non-pathogenic rickettsiae.Infection and immunity · 2025Article
- Development of a Recombinase-Mediated Cassette Exchange System for Gene Knockout and Expression of Non-Native Gene Sequences inVaccines · 2025Article
- Pathogenic rickettsiae encode a secreted lipase that facilitates intracytosolic colonization in host cells.PloS one · 2025Article
- Development of inducible promoter and CRISPRi plasmids functional inJournal of bacteriology · 2024Article
- An expanded genetic toolkit for inducible expression and targeted gene silencing inJournal of bacteriology · 2024Article
- Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen.Nature communications · 2024Article
- An expanded genetic toolkit for inducible expression and targeted gene silencing inbioRxiv : the preprint server for biology · 2024Article
- PathogenicJournal of bacteriology · 2024Review
- Critical roles ofInfection and immunity · 2024Article
- Metabolism and physiology of pathogenic bacterial obligate intracellular parasites.Frontiers in cellular and infection microbiology · 2024Review
- Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen.bioRxiv : the preprint server for biology · 2023Article
- Advances in genetic manipulation ofFrontiers in immunology · 2023Review
- Recent advances in genetic systems in obligate intracellular human-pathogenic bacteria.Frontiers in cellular and infection microbiology · 2023Review
- Pathogenicity and virulence ofVirulence · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledStrains of Rickettsia rickettsii, the causative agent of Rocky Mountain spotted fever (RMSF), differ dramatically in virulence despite >99% genetic homology. Spotted fever group (SFG) rickettsiae produce two immunodominant outer membrane proteins, rickettsial OmpA (rOmpA) and rOmpB, which are conserved throughout the SFG and thought to be fundamental to pathogenesis. rOmpA is present in all virulent strains of R. rickettsii but is not produced in the only documented avirulent strain, Iowa, due to a premature stop codon. Here we report the creation of an isogenic ompA mutant in the highly virulent strain Sheila Smith by insertion of intronic RNA to create a premature stop codon 312 bp downstream of the 6,747-bp open reading frame initiation site (int312). Targeted insertion was accomplished using an LtrA group II intron retrohoming system. Growth and entry rates of Sheila Smith ompA::int312 in Vero cells remained comparable to those of the wild type. Virulence was assessed in a guinea pig model by challenge with 100 PFU of either ompA::int312 Sheila Smith or the wild type, but no significant difference in either fever peak (40.5°C) or duration (8 days) were shown between the wild type and the knockout. The ability to disrupt genes in a site-specific manner using an LtrA group II intron system provides an important new tool for evaluation of potential virulence determinants in rickettsial disease research. IMPORTANCE: R. rickettsii rOmpA is an immunodominant outer membrane autotransporter conserved in the spotted fever group. Previous studies and genomic comparisons suggest that rOmpA is involved in adhesion and may be critical for virulence. Little information is available for rickettsial virulence factors in an isogenic background, as limited systems for targeted gene disruption are currently available. Here we describe the creation of an rOmpA knockout by insertion of a premature stop codon into the 5' end of the open reading frame using a group II intron system. An isogenic rOmpA knockout mutation in the highly virulent Sheila Smith strain did not cause attenuation in a guinea pig model of infection, and no altered phenotype was observed in cell culture. We conclude that rOmpA is not critical for virulence in a guinea pig model but may play a role in survival or transmission from the tick vector.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.