title: Burkholderia Hep_Hag autotransporter (BuHA) proteins elicit a strong antibody response during experimental glanders but not human melioidosis.
abstract: BACKGROUND
  The bacterial biothreat agents Burkholderia mallei and Burkholderia pseudomallei are the cause of glanders and melioidosis, respectively. Genomic and epidemiological studies have shown that B. mallei is a recently emerged, host restricted clone of B. pseudomallei.
  
  
  RESULTS
  Using bacteriophage-mediated immunoscreening we identified genes expressed in vivo during experimental equine glanders infection. A family of immunodominant antigens were identified that share protein domain architectures with hemagglutinins and invasins. These have been designated Burkholderia Hep_Hag autotransporter (BuHA) proteins. A total of 110/207 positive clones (53%) of a B. mallei expression library screened with sera from two infected horses belonged to this family. This contrasted with 6/189 positive clones (3%) of a B. pseudomallei expression library screened with serum from 21 patients with culture-proven melioidosis.
  
  
  CONCLUSIONS
  Members of the BuHA proteins are found in other Gram-negative bacteria and have been shown to have important roles related to virulence. Compared with other bacterial species, the genomes of both B. mallei and B. pseudomallei contain a relative abundance of this family of proteins. The domain structures of these proteins suggest that they function as multimeric surface proteins that modulate interactions of the cell with the host and environment. Their effect on the cellular immune response to B. mallei and their potential as diagnostics for glanders requires further study.
authors.affiliation: Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. rachaneeporn_t@hotmail.com <rachaneeporn_t@hotmail.com>
authors.forename: Rachaneeporn
authors.initials: R
authors.lastname: Tiyawisutsri
authors.forename: Matthew T G
authors.initials: MT
authors.lastname: Holden
authors.forename: Sarinna
authors.initials: S
authors.lastname: Tumapa
authors.forename: Sirirat
authors.initials: S
authors.lastname: Rengpipat
authors.forename: Simon R
authors.initials: SR
authors.lastname: Clarke
authors.forename: Simon J
authors.initials: SJ
authors.lastname: Foster
authors.forename: William C
authors.initials: WC
authors.lastname: Nierman
authors.forename: Nicholas P J
authors.initials: NP
authors.lastname: Day
authors.forename: Sharon J
authors.initials: SJ
authors.lastname: Peacock
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis* / Q000276:immunology; D000942:Antigens, Bacterial / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D001425:Bacterial Outer Membrane Proteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology*; D001483:Base Sequence; D042726:Burkholderia mallei / Q000235:genetics / Q000276:immunology*; D016957:Burkholderia pseudomallei / Q000235:genetics / Q000276:immunology*; D002648:Child; D005260:Female; D015723:Gene Library; D005896:Glanders / Q000175:diagnosis / Q000276:immunology* / Q000382:microbiology; D006388:Hemagglutinins / Q000276:immunology; D006736:Horses; D006801:Humans; D008297:Male; D008554:Melioidosis / Q000097:blood / Q000276:immunology* / Q000382:microbiology; D008875:Middle Aged; D008969:Molecular Sequence Data; D037521:Virulence Factors / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins; D006388:Hemagglutinins; D037521:Virulence Factors