Genetic alterations of Streptococcus mutans' virulence.
The use of mutants defective in caries-associated traits has enabled the genetic dissociation of agglutination from adhesion, the demonstration of serotype-specific contributions of IPS to virulence, the importance of glucanohydrolase to virulence to a greater degree than to plaque formation, and the apparent lack of importance of agglutination to virulence. We have also been able to demonstrate the ability of plaque formation-defective mutants and other variants both to infect and to emerge, yet not to cause disease. Additional mutants, currently under study in our laboratory include fructanase, invertase, and sucrose permease-defectives. Ultimately, the identification of key, probably surface-associated virulence factors will offer more potent and specific antigens for directed immune responses by the host.
D000268:Adhesiveness; D000818:Animals; D003731:Dental Caries / Q000382:microbiology*; D003910:Dextranase / Q000378:metabolism; D005936:Glucans / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D011135:Polysaccharides, Bacterial / Q000378:metabolism; D051381:Rats; D013295:Streptococcus mutans / Q000235:genetics / Q000472:pathogenicity*
D005936:Glucans; D011135:Polysaccharides, Bacterial; D003910:Dextranase