
Researchers at Virginia Commonwealth University (VCU) discovered an enzyme, lactate dehydrogenase (BbLDH), as a potential therapeutic target for Lyme disease.
This enzyme plays a pivotal role in enabling the infectivity and survival of Borrelia burgdorferi, the bacteria that causes Lyme disease.
The study is published in mBio, the journal of the American Society of Microbiology.
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The VCU’s School of Dentistry’s MD and study author Chunhao (Chris) Li stated: “We discovered that BbLDH has a unique biochemical and structural feature and it is essential for B. burgdorferi growth and infectivity.”
Lyme disease is caused by the bite of an infected deer tick. It is the most commonly reported tick-borne disease in the U.S. and Europe, affecting hundreds of thousands of individuals every year.
The bacterium B. burgdorferi consists of numerous distinctive mechanisms to grow in diverse environments such as in the body of a tick and a mammalian host.
The BbLDH’s discovery as a therapeutic target relied on previous research which was conducted by the VCU researchers.
It showed that B. burgdorferi does not use thiamine, a cofactor which is used by numerous mechanisms, but instead, it depends on lactate dehydrogenase to convert pyruvate to lactate and maintain an NADH/NAD+ ratio.
It's a great metabolic pathway essential to maintain this energy production.
In addition, the researchers used an integrated approach combining biochemistry, and genetics, and then performed loss-of-function studies to reveal the significance of BbDLH in the infectivity and growth of B. burgdorferi.
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