Researchers at the University of California San Francisco and Johns Hopkins studied the molecular basis of Lyme disease and found that early infection has a distinctive gene expression profile that lasts for weeks, a molecular pattern that may be characteristic of other infections, such as chronic hepatitis C.
The research paper, “Longitudinal Transcriptome Analysis Reveals a Sustained Differential Gene Expression Signature in Patients Treated for Acute Lyme Disease,” was published in mBio, a journal published by The American Society for Microbiology.
Lyme disease is the most common tick-borne infection in the United States. It is caused by the bacterium Borrelia burgdorferi, and a significant number of patients, approximately 10 percent to 20 percent, report lingering symptoms months to years after proper treatment with antibiotics. According to the Centers for Disease Control and Prevention (CDC), some 30,000 cases of Lyme disease are reported each year in the U.S. However, Lyme disease is difficult to diagnose and experts predict that many more cases go undiagnosed, especially because most diagnoses are made through surveillance of symptoms.
Researchers aimed in this study to better understand the role of the host’s gene expression profile response to infection, and to gain insight into the development and maintenance of symptoms even after treatment. They investigated the transcriptome (gene expression) of 29 Lyme disease patients and 13 matched controls, from diagnosis until six months after treatment.
The scientists found that the gene expression signature of early Lyme disease is distinct from other acute infectious diseases and lasts for at least three weeks after infection. In people with Lyme disease, less than 44 percent of differentially expressed genes were also expressed in other syndromes. Some of these differences in the transcriptome persisted for six months after treatment, although after that time Lyme disease patients were found to have 31 percent to 60 percent of their pathways in common with other immune-mediated diseases, such as systematic lupus erythematosus, rheumatoid arthritis, and chronic fatigue syndrome.
Dr. John Aucott, MD, the study’s senior investigator and an assistant professor of medicine at the Johns Hopkins University School of Medicine, said in a press release, “To our knowledge, this study is the first to document changes in gene expression occurring even after a bacterial infection has been treated with appropriate antibiotics.”
Importantly, this study uncovered many previously unknown molecular pathways, and researchers believe many of these genes and pathways may be useful in the future as clinical biomarkers for earlier diagnosis and potential targets for new therapies.