| Summary: | 碩士 === 長庚大學 === 基礎醫學研究所 === 93 === 英文摘要
The virulence antigen, Vi first described by Felix and Pitt in 1934, is a capsular surface antigen consisting of a homopolymer of N-acetyl-galactosamine uronic acid. Vi antigen expressing forms appeared as dense, bright and orange-tinted colonies, readily distinguishable from the dull, translucent colonies of the Vi non-expressing forms.
This antigen is an indispensable virulence factor of Salmonella enterica serovar Typhi. Several other Salmonella enterica serovar such as Paratyphi C, Dublin and Citrobacter freundii also express Vi antigen. The expression of Vi antigen in Salmonella Typhi and Paratyphi C is generally stable. In constrast, the Vi antigen expression in C. freundii characteristically undergoes a rapid, reversible transition between the Vi-producing state and the Vi-nonproducing state.
To verify whether the switching phenotype is due to alteration on the structure genes (Vi), the viaB operon was expressed in Vi+ and Vi- background or a moderate-copy plasmid (pWR127). When the restriction endonucleas digestion pattern of pWR127 from Vi+ stage and Vi- stage bacteria were compared, no alteration was detected, indicating there was little difference in nucleotide sequence. Thus the Vi+ and Vi- switching phenotype is not regulated at the viaB region.
To investigate the mechanism of switching, mutants that are deficient in switching Vi expression were generate by transposon mutagenesis. Three such clones, designed as SwcA, B and C, with mutations in waaD, waaF and waaL, respectingly, were subsequently identified. Interestingly, all three genes are involved in lipopolysaccharied (LPS) synthesis, and do not possess any known regulating function. How genes affect capsular antigen Vi expression is unknow.
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