May 27, 1999 Researchers at the University of Maryland School of Medicine have found that some bacterial structures and disease-causing genes actually come from viruses, which have integrated into the bacterial cell. The discovery alters the understanding of the emergence and pathogenesis of bacterial diseases, and could lead to new vaccines for diseases like cholera.
"We have discovered a key factor in the emergence of many epidemic bacterial pathogens," says David K.R. Karaolis, PhD, of the Division of Hospital Epidemiology. "It's like a virus conspiracy that turns otherwise peaceful bacterial strains into serious pathogens."
Karaolis and colleagues discovered that:
* The bacterium Vibrio cholerae (which causes cholera) contains a cluster of genes that actually comes from a virus, which the authors named VPIphi. These genes are necessary for cholera infection;
* surface structures thought to be part of V. cholerae are actually copies of VPIphi;
* VPIphi acts as a receptor for a second virus, CTXphi, which contains the genes for the cholera toxin. Only after receiving both viruses can a strain of V. cholerae cause disease.
The results are published in the May 27 issue of the journal Nature.
Most disease-causing bacteria have a cluster of genes called a "pathogenicity island," which contains genes that control and contribute to disease. Until now, the origins and transferability of these gene clusters was uncertain.
"This implies that pathogenicity islands in other bacteria may come from viruses," says Karaolis, who completed much of the research while a part of the University of Maryland's Center for Vaccine Development.
The researchers also found that surface structures on V. cholerae called type IV pili, essential for colonization of the bacteria's host, are actually copies of VPIphi's protein coat. Secreted by the bacteria, the virus can act as a receptor for the cholera toxin virus. Similar surface structures are found on many other bacterial pathogens.
"To find that one virus controls another virus is remarkable," says Karaolis.
In tracing the evolution of cholera, the study shows that when a harmless strain of Vibrio cholerae becomes infected by VPIphi, the viral genes integrate into the bacterium. That strain can now produce copies of this virus, which are presented on the bacterial cell membrane and act as receptors for the cholera toxin virus, CTXphi. The toxin virus can now attach to the bacterium and inject its genes, creating a cell capable of causing cholera.
Karaolis, a native of Sydney, Australia, researches the genetic factors and mechanisms involved in the emergence, pathogenesis and spread of epidemic diseases such as cholera. He recently received a Burroughs Wellcome Fund Career Award in the biomedical sciences.
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