Abstract
Borrelia burgdorferi sensu lato causes Lyme borreliosis in a variety of animals and humans. These atypical bacterial pathogens are maintained in a complex enzootic life cycle that primarily involves a vertebrate host and Ixodes spp. ticks. In the Northeastern United States, I. scapularis is the main vector, while wild rodents serve as the mammalian reservoir host. As B. burgdorferi is transmitted only by I. scapularis and closely related ticks, the spirochete-tick interactions are thought to be highly specific. Various borrelial and arthropod proteins that directly or indirectly contribute to the natural cycle of B. burgdorferi infection have been identified. Discrete molecular interactions between spirochetes and tick components also have been discovered, which often play critical roles in pathogen persistence and transmission by the arthropod vector. This review will focus on the past discoveries and future challenges that are relevant to our understanding of the molecular interactions between B. burgdorferi and Ixodes ticks. This information will not only impact scientific advancements in the research of tick- transmitted infections but will also contribute to the development of novel preventive measures that interfere with the B. burgdorferi life cycle.
| Original language | English |
|---|---|
| Pages (from-to) | 113-144 |
| Number of pages | 32 |
| Journal | Current Issues in Molecular Biology |
| Volume | 42 |
| DOIs | |
| State | Published - 2021 |
Funding
The authors are thankful to Kathryn Nassar for assistance with the preparation of this review. We are grateful to Aravinda M. de Silva, Deborah Shroder, and Ireen Dryburgh-Barry for assistance with the preparation of the original manuscript. Lymedisease research in our laboratories is supported by several past and ongoing funding supports from the National Institutes of Health (including currently active grants, P01AI138949 and R01AI154542 to U.P), the Department of Defense, Global LymeAlliance, Merck & Co. Inc., the Arthritis Foundation, the American Heart Association, and the Steven and Alexandra Cohen Foundation. Erol Fikrig is an Investigator of the Howard Hughes Medical Institute. Chrysoula Kitsou is the recipient of the Deborah and Mark Blackman Postdoctoral Fellowship from Global Lyme Alliance. The authors are thankful to Kathryn Nassar for assistance with the preparation of this review. We are grateful to Aravinda M. de Silva, Deborah Shroder, and Ireen Dryburgh-Barry for assistance with the preparation of the original manuscript. Lyme disease research in our laboratories is supported by several past and ongoing funding supports from the National Institutes of Health (including currently active grants, P01AI138949 and R01AI154542 to U.P), the Department of Defense, Global Lyme Alliance, Merck & Co. Inc., the Arthritis Foundation, the American Heart Association, and the Steven and Alexandra Cohen Foundation. Erol Fikrig is an Investigator of the Howard Hughes Medical Institute. Chrysoula Kitsou is the recipient of the Deborah and Mark Blackman Postdoctoral Fellowship from Global Lyme Alliance.
| Funders | Funder number |
|---|---|
| Merck | |
| P01AI138949 | |
| Howard Hughes Medical Institute | |
| R01AI154542 | |
| American Heart Association | |
| Arthritis Foundation | |
| Merck | |