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Infect Immun, June 1998, p. 2535-2539, Vol. 66, No. 6
Department of Molecular Microbiology and
Immunology, School of Medicine, University of Missouri
Received 16 January 1998/Returned for modification 4 March
1998/Accepted 20 March 1998
We previously isolated from a 1994 isolate of Vibrio
cholerae O139 a filamentous lysogenic bacteriophage, choleraphage
493, which inhibits pre-O139 but not post-O139 El Tor biotype V. cholerae strains in plaque assays. We investigated the role of
the mannose-sensitive hemagglutinin (MSHA) type IV pilus as a receptor
in phage 493 infection. Spontaneous, Tn5 insertion, and
mshA deletion mutants are resistant to 493 infection.
Susceptibility is restored by mshA complementation of
deletion mutants. Additionally, the 493 phage titer is reduced by
adsorption with MSHA-positive strains but not with a
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Copyright © 1998, American Society for Microbiology. All rights reserved.
The Vibrio cholerae Mannose-Sensitive
Hemagglutinin Is the Receptor for a Filamentous Bacteriophage
from V. cholerae O139
Columbia,
Columbia, Missouri 65212,1 and
Department of Microbiology, Dartmouth Medical
School, Hanover, New Hampshire 03755-38422
mshA1 strain. Monoclonal antibody against MSHA inhibits
plaque formation. We conclude that MSHA is the receptor for phage 493. The emergence and decline of O139 in India and Bangladesh are
correlated with the susceptibility and resistance of El Tor strains to
493. However, mshA gene sequences of post-O139 strains are
identical to those of susceptible pre-O139 isolates, indicating that
phage resistance of El Tor is not due to a change in mshA.
Classical biotype strains are (with rare exceptions) hemagglutinin
negative and resistant to 493 in plaque assays. Nevertheless, they
express the mshA pilin gene. They can be infected with 493 and produce low levels of phage DNA, like post-O139 El Tor strains.
Resistance to 493 in plaque assays is thus not equivalent to resistance
to infection. The ability of filamentous phages, such as 493, to
transfer large amounts of DNA provides them, additionally, with the
potential for quantum leaps in both identity and pathogenicity, such as
the conversion of El Tor to O139.
*
Corresponding author. Mailing address: Department of
Molecular Microbiology and Immunology, School of Medicine, DC 385.00, Allton Bldg. 208, University of Missouri
Columbia, 301 Business Loop
70 West, Columbia, MO 65212. Phone: (573) 882-4117. Fax: (573)
884-7885. E-mail: rfinkels{at}mail.coin.missouri.edu.
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