8
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Outer surface protein polymorphisms linked to host‐spirochete association in Lyme borreliae

      1 , 2 , 3 , 4 , 5 , 1 , 3 , 6
      Molecular Microbiology
      Wiley

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          <p id="P4">Lyme borreliosis is caused by multiple species of the spirochete bacteria <i>Borrelia burgdorferi</i> sensu lato. The spirochetes are transmitted by ticks to vertebrate hosts including small and mediumsized mammals, birds, reptiles, and humans. Strain-to-strain variation in host specific infectivity has been documented, but the molecular basis that drives this differentiation is still unclear. Spirochetes possess the ability to evade host immune responses and colonize host tissues to establish infection in vertebrate hosts. In turn, hosts have developed distinct levels of immune responses when invaded by different species/strains of Lyme borreliae. Similarly, the ability of Lyme borreliae to colonize host tissues varies among different spirochete species/strains. One potential mechanism that drives this strain-to-strain variation of immune evasion and colonization is the polymorphic outer surface proteins produced by Lyme borreliae. In this review, we summarize research on strain-to-strain variation in host competence and discuss the evidence that supports the role of spirocheteproduced protein polymorphisms in driving this variation in host specialization. Such information will provide greater insights into the adaptive mechanisms driving host and Lyme borreliae association, which will lead to the development of interventions to block pathogen spread and eventually reduce Lyme borreliosis health burden. </p><p id="P5"> <div class="figure-container so-text-align-c"> <img alt="" class="figure" src="/document_file/1fcf8584-a0e5-448f-8eb0-21c3f4941532/PubMedCentral/image/nihms-1009195-f0001.jpg"/> </div> </p><p id="P6">Lyme disease causing bacteria species are transmitted between ticks and different vertebrate hosts including mammals, birds, and reptiles, and different bacteria species are associated with different hosts. Potential mechanisms driving these bacteria-host associations include: strain-to-strain differences in the induced innate and adaptive immune response and bacteria protein variants that display differentially binding activity to cells. </p>

          Related collections

          Most cited references156

          • Record: found
          • Abstract: found
          • Article: not found

          Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi.

          The genome of the bacterium Borrelia burgdorferi B31, the aetiologic agent of Lyme disease, contains a linear chromosome of 910,725 base pairs and at least 17 linear and circular plasmids with a combined size of more than 533,000 base pairs. The chromosome contains 853 genes encoding a basic set of proteins for DNA replication, transcription, translation, solute transport and energy metabolism, but, like Mycoplasma genitalium, it contains no genes for cellular biosynthetic reactions. Because B. burgdorferi and M. genitalium are distantly related eubacteria, we suggest that their limited metabolic capacities reflect convergent evolution by gene loss from more metabolically competent progenitors. Of 430 genes on 11 plasmids, most have no known biological function; 39% of plasmid genes are paralogues that form 47 gene families. The biological significance of the multiple plasmid-encoded genes is not clear, although they may be involved in antigenic variation or immune evasion.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Of ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes.

            In little more than 30 years, Lyme disease, which is caused by the spirochaete Borrelia burgdorferi, has risen from relative obscurity to become a global public health problem and a prototype of an emerging infection. During this period, there has been an extraordinary accumulation of knowledge on the phylogenetic diversity, molecular biology, genetics and host interactions of B. burgdorferi. In this Review, we integrate this large body of information into a cohesive picture of the molecular and cellular events that transpire as Lyme disease spirochaetes transit between their arthropod and vertebrate hosts during the enzootic cycle.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Epidemiology of Lyme disease.

              Lyme disease is the most common vector-borne illness in North America and Europe. The etiologic agent, Borrelia burgdorferi sensu lato, is transmitted to humans by certain species of Ixodes ticks, which are found widely in temperate regions of the Northern hemisphere. Clinical features are diverse, but death is rare. The risk of human infection is determined by the geographic distribution of vector tick species, ecologic factors that influence tick infection rates, and human behaviors that promote tick bite. Rates of infection are highest among children 5 to 15 years old and adults older than 50 years.
                Bookmark

                Author and article information

                Journal
                Molecular Microbiology
                Mol Microbiol
                Wiley
                0950-382X
                1365-2958
                February 28 2019
                April 2019
                February 27 2019
                April 2019
                : 111
                : 4
                : 868-882
                Affiliations
                [1 ]Department of Ecology, Evolution, and Environmental Biology Columbia University New York NY USA
                [2 ]Department of Biological Sciences University at Albany Albany NY USA
                [3 ]Division of Infectious Diseases, Wadsworth Center New York State Department of Health Albany NY USA
                [4 ]Department of Biology Misericordia University Dallas PA USA
                [5 ]Department of Epidemiology and Biostatistics, School of Public Health SUNY Downstate Medical Center Brooklyn NY USA
                [6 ]Department of Biomedical Sciences University at Albany Albany NY USA
                Article
                10.1111/mmi.14209
                6510028
                30666741
                29022978-3d2d-4fa0-80e2-ccceeebcf15c
                © 2019

                http://onlinelibrary.wiley.com/termsAndConditions#am

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

                History

                Comments

                Comment on this article