Pathogenic neisseriae--a model of bacterial virulence and genetic flexibility

The outcome of the early stages of a neisserial infection is determined by receptor-mediated events that culminate in the attachment and invasion of human mucosal tissues. The factors participating in this process, including pili, opacity proteins (Opa), and perhaps lipopolysaccharide (LPS), are subject to complex genetic controls that allow these factors to be produced in multiple forms. Antigenic variation allows the pathogenic Neisseriae to evade the human immune response, and facilitates their interaction with a variety of different cells and tissues of the human host. One of the major genetic mechanisms causing antigenic variation is transformation, which allows virulence genes to be exchanged and recombined between independent Neisseria strains within multiply infected individuals. A number of other factors, such as IgA protease, alpha-factor, and the meningococcal capsule are also implicated in pathogenesis and render the pathogenic Neisseriae an excellent model for the investigation of bacterial virulence.