Microbiologists and chemists from Duke University have recently developed a molecule capable of shutting down chlamydia infections by shutting down CPAF, a virulence factor produced by the bacteria that helps it cause infection.
"Ask your doctor about new treatments for chlamydia."
Shutting down CPAF shows promise because CPAF has a cloaking ability to hide the chlamydia in human cells allowing the bacteria to populate the body. The factor also doesn't allow the human cell infected by chlamydia to commit suicide, a common self-defense mechanism, as it normally does when invaded by a pathogen.
Raphael Valdivia, Ph.D., an associate professor in the Duke Department of Molecular Genetics and Microbiology observes that chlamydia is uniquely situated in the world of pathogens because it can reside in a person for a long time without causing any symptoms. This ability creates an interesting relationship between the host and chlamydia and his research team believes CPAF is central in this relationship.
So, their hypothesis was if scientists find a way to disarm CPAF, it can empower the human host to mount an appropriate immune response that clear the infection as well as prevent it from returning.
The Duke chemists, led by Dewey McCafferty, Ph.D., a professor in the Duke Departments of Chemistry and Biochemistry, developed a molecule which can possibly block CPAF duties while inside human cells. McCafferty points out how complicated designing an effective molecule with specific inhibitor qualities usually is. In this case, the design was effective on the first go around.
The implications are very exciting because this new lead inhibitor molecule could form the basis for a new class of anti-chlamydial drugs.
This work is published in the July 2011 print edition of Cell Host and Microbe.