Outer Surface Protein B Is Critical for Borrelia burgdorferi Adherence and Survival within Ixodes Ticks
Open Access
- 9 March 2007
- journal article
- research article
- Published by Public Library of Science (PLoS) in PLoS Pathogens
- Vol. 3 (3) , e33
- https://doi.org/10.1371/journal.ppat.0030033
Abstract
Survival of Borrelia burgdorferi in ticks and mammals is facilitated, at least in part, by the selective expression of lipoproteins. Outer surface protein (Osp) A participates in spirochete adherence to the tick gut. As ospB is expressed on a bicistronic operon with ospA, we have now investigated the role of OspB by generating an OspB-deficient B. burgdorferi and examining its phenotype throughout the spirochete life cycle. Similar to wild-type isolates, the OspB-deficient B. burgdorferi were able to readily infect and persist in mice. OspB-deficient B. burgdorferi were capable of migrating to the feeding ticks but had an impaired ability to adhere to the tick gut and survive within the vector. Furthermore, the OspB-deficient B. burgdorferi bound poorly to tick gut extracts. The complementation of the OspB-deficient spirochete in trans, with a wild-type copy of ospB gene, restored its ability to bind tick gut. Taken together, these data suggest that OspB has an important role within Ixodes scapularis and that B. burgdorferi relies upon multiple genes to efficiently persist in ticks. Lyme disease is the most common vector-borne disease in North America and Europe. The causative agent Borrelia burgdorferi is a bacterium that is maintained in an enzoonotic cycle between Ixodes ticks and a large range of mammals. Accidental encounters of infected Ixodes ticks with humans results in the transmission of B. burgdorferi and subsequent Lyme disease. Given that global control efforts have met with limited success, the need for developing novel interventions to combat this infection has become all the more vital. A better understanding of how B. burgdorferi interacts with its vector might lead to new ideas for combating the Lyme disease. B. burgdorferi upregulates outer surface protein (Osp) A and B during entry into ticks, and OspA contributes to the colonization of bacterium within the vector gut. We now demonstrate that OspB also facilitates the colonization and survival of B. burgdorferi in ticks. This work provides the basis for future studies as to how this protein facilitates interaction of B. burgdorferi to the tick gut and thus ultimately a basis for the development of novel strategies to interrupt the spirochete life cycle.Keywords
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