Abstract

Bordetella pertussis produces a series of virulence factors that are involved in one of several steps of the pathogenesis of whooping cough. By comparison to other infectious diseases, such as diphtheria or tetanus, pertussis has initially been viewed as a mere toxin-mediated disease in which pertussis toxin plays the major key role. However, it is now clear that the expression of the disease requires numerous virulence factors that have classically been subdivided into adhesins and toxins. The major adhesins are filamentous haemagglutinin, pertactin and the fimbriae, and the major toxins are pertussis toxin, adenylate cyclase and dermonecrotic toxin, in addition to non-protein toxins, such as tracheal cytotoxin and lipopolysaccharide. In addition to their function as individual virulence factors, adhesins and toxins may also act in synergy to favour efficient B. pertussis infection. More recently, new approaches to the study of virulence, essentially based on genomics, have revealed that the molecular mechanisms of B. pertussis virulence is far more complex than initially assumed, and that it involves additional virulence factors. The production of most, but not all of these factors is under the control of a two-component regulatory system named BvgA/S. This system is able to sense signals from the environment and transmit this information via a phosphorylation cascade to a transcriptional activator. The phosphorylated activator can then, in turn, induce the expression of the various virulence genes. The precise role of the newly identified virulence factors is not yet known, but will undoubtedly be the focus of future studies.

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