THE VIBRIO-CHOLERAE MANNOSE-SENSITIVE HEMAGGLUTININ IS THE RECEPTOR FOR A FILAMENTOUS BACTERIOPHAGE FROM VIBRIO-CHOLERAE O139

We previously isolated from a 1994 isolate of Vibrio cholerae 0139 a f ilamentous lysogenic bacteriophage, choleraphage 493, which inhibits p re-0139 but not post-0139 El Tor biotype V. cholerae strains in plaque assays. We investigated the role of the mannose-sensitive hemagglutin in (MSH[A) type IV pilus as a receptor in phage 493 infection. Spontan eous, Tn5 insertion, and mshA deletion mutants are resistant to 493 in fection. Susceptibility is restored by mshA complementation of deletio n mutants. Additionally, the 493 phage titer is reduced by adsorption with MSHA-positive strains but not with a Delta mshAl strain. Monoclon al antibody against MSHA inhibits plaque formation. We conclude that M SHA is the receptor for phage 493, The emergence and decline of 0139 i n India and Bangladesh are correlated with the susceptibility and resi stance of El Tor strains to 493. However, mshA gene sequences of post- 0139 strains are identical to those of susceptible pre-0139 isolates, indicating that phage resistance of El Tor is not due to a change in m shA. Classical biotype strains are (with rare exceptions) hemagglutini n negative and resistant to 493 in plaque assays. Nevertheless, they e xpress the mshA pilin gene. They can be infected with 493 and produce low levels of phage DNA, like post-0139 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 am ounts of DNA provides them, additionally, with the potential for quant um leaps in both identity and pathogenicity, such as the conversion of El Tor to 0139.