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      <item>
        <name>
          <family>Li</family>
          <given>M</given>
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      </item>
      <item>
        <name>
          <family>Kotetishvili</family>
          <given>M</given>
        </name>
        <id>mamuka_kotetishvili@iliauni.edu.ge</id>
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        <name>
          <family>Chen </family>
          <given>Y</given>
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          <family>Sozhamannan</family>
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    <title>Comparative genomic analyses of
the vibrio pathogenicity island and cholera toxin prophage regions in nonepidemic
serogroup strains of Vibrio cholerae</title>
    <ispublished>pub</ispublished>
    <subjects>
      <item>R1</item>
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    <abstract>Two major virulence factors are associated with epidemic strains (O1 and O139
serogroups) of Vibrio cholerae: cholera toxin encoded by the ctxAB genes and
toxin-coregulated pilus encoded by the tcpA gene. The ctx genes reside in the
genome of a filamentous phage (CTXphi), and the tcpA gene resides in a vibrio
pathogenicity island (VPI) which has also been proposed to be a filamentous phage
designated VPIphi. In order to determine the prevalence of horizontal transfer of
VPI and CTXphi among nonepidemic (non-O1 and non-O139 serogroups) V. cholerae,
300 strains of both clinical and environmental origin were screened for the
presence of tcpA and ctxAB. In this paper, we present the comparative genetic
analyses of 11 nonepidemic serogroup strains which carry the VPI cluster. Seven
of the 11 VPI(+) strains have also acquired the CTXphi. Multilocus sequence
typing and restriction fragment length polymorphism analyses of the VPI and
CTXphi prophage regions revealed that the non-O1 and non-O139 strains were
genetically diverse and clustered in lineages distinct from that of the epidemic 
strains. The left end of the VPI in the non-O1 and non-O139 strains exhibited
extensive DNA rearrangements. In addition, several CTXphi prophage types
characterized by novel repressor (rstR) and ctxAB genes and VPIs with novel tcpA 
genes were found in these strains. These data suggest that the potentially
pathogenic, nonepidemic, non-O1 and non-O139 strains identified in our study most
likely evolved by sequential horizontal acquisition of the VPI and CTXphi
independently rather than by exchange of O-antigen biosynthesis regions in an
existing epidemic strain.</abstract>
    <date>2003</date>
    <publication>Appl Environ Microbiol</publication>
    <refereed>TRUE</refereed>
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