MODULATION OF VIRULENCE FACTORS Bacteria which cause disease have special factors which are designated as virulence factors. These factors contribute to the virulence of the microorganisms and to their survival in the hostile envirnoment within the body of their host. Various signals control the expression of the virulence factors. Oxygen, temperature, concentration of ions, and pH are some of the known signals that change the bacterial virulence. Pettersson et al and Zhang and Normark, provide the evidence in the August issue of Science that bacteria-host cell contact plays a major role in controlling the virulence of bacteria by changing the expression of virulence factors. Pettersson et al examined the control of the virulence factor in the Yersinia pseudotuberculosis. Yersinia includes such virulent bacteria as Yersinia pestis (1), the cause of plague, as well as Yersinia enterocolitica (1,2, 3) and Yersinia pseudotuberculosis (1)which both cause gastrointestinal infection. The virulence of these microorganisms is due to the secretion of virulence factors that are called Yops. These include: 1. YpkA, a kinase homologus to eukaryotes serine and threonine kinases 2. YopE, a cytotoxic factor which causes depolymerization of actin 3. YopH, a protein tyrosine phosphatase Yops are encoded by a common, 70-kb, plasmid and their expression is exquisitely controlled by various envirnomental factors. For example, in presence of high Ca2+, the amount of secreted Yops is low. On the other hand, in the absence of Ca2+, the transcription of the Yops begins and large amount of Yops is secreted. Pettersson et al measured the virulence of the Yersinia pseudotuberculosis by monitoring the emission of light from bacteria that expressed luciferase gene. Luciferase was under the control of ypoE promoter. Contact with the host cells triggered an increased expression of Yops. Zhang and Normark also reached the conclusion that bacteria-host cell interaction is required for manifestation of virulence by the bacteria. Escherichia coli can cause urinary tract infection. P-pilli on these bacteria mediates their binding to the P blood group antigens on the host epithelial cells and therefore, allow development of urinary tract infection. Zhang and Normark showed that this binding initiates transcription of a sensor-regulator protein. Mutation of the sensor-regulator gene led to the inability of the E coli to grow in urine. These findings show that the virulence of bacteria is regulated by their interaction with the host cells. REFERENCES: Pettersson J, Nordfelth R, Dubinina E, Bergman T, Gustaffsson M, Magnusson KE, Wolf-Watz H: Modulation of virulence factor by pathogen target cell contact. Science 273, 1231-1233, 1996 Zhang JP, Normark S: Induction of gene expression in Escherichia coli after pilus-mediated adherence. Science 273, 1234-1236, 1996 RESOURCES : Microbiology Resources Immunodetection of Virulent Strains of Yersinia Enterocolitica Using a Single