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Interaction between bacteriophage Sf6 and Shigella flexner.

A A Lindberg, R Wollin, P Gemski

    Journal of Virology
    |July 1, 1978
    PubMed
    Summary
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    Shigella flexneri phage Sf6 possesses alpha-1,3-endorhamnosidase activity, cleaving specific O-polysaccharide structures. Acetylation of the S. flexneri O-group 3,4 antigen blocks this enzymatic hydrolysis.

    Area of Science:

    • Bacteriophage research
    • Microbial genetics
    • Glycobiology

    Background:

    • Shigella flexneri is a Gram-negative bacterium causing bacillary dysentery.
    • Bacteriophages, viruses that infect bacteria, are crucial in microbial ecology and evolution.
    • Phage Sf6, a C-group phage, exhibits specific lytic activity against S. flexneri.

    Purpose of the Study:

    • To characterize the enzymatic activity of Shigella flexneri phage Sf6.
    • To elucidate the substrate specificity of the phage's endorhamnosidase.
    • To investigate the role of O-polysaccharide acetylation in phage-bacterial interactions.

    Main Methods:

    • Morphological characterization of phage Sf6.
    • Enzymatic assays using methylation and reducing end group sugar analyses.

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  • Interaction studies with S. flexneri O-polysaccharide chains (O-group 3,4 antigen).
  • Analysis of hydrolysis products and the effect of acetylation/deacetylation.

    • Main Results:

    • Phage Sf6 has an isometric head (53nm) and long noncontractile tails.
    • The phage possesses alpha-1,3-endorhamnosidase activity, hydrolyzing the S. flexneri O-polysaccharide.
    • The major hydrolysis product is an octasaccharide: Rha III-GlcNAc-Rha I-Rha II-Rha III-GlcNAc-Rha I-Rha II.
    • Acetylation of rhamnose III at O-2 prevents enzymatic hydrolysis; O-deacetylation restores susceptibility.

    Conclusions:

    • Phage Sf6's endorhamnosidase specifically targets the O-group 3,4 antigen of S. flexneri.
    • O-acetylation of the O-polysaccharide is a key mechanism of resistance against phage Sf6.
    • Understanding these interactions can inform phage therapy and bacterial evasion strategies.