Molecular Interactions During Borrelia burgdorferi Migration from the Vector to the Mammalian Nervous System

Curr Protein Pept Sci. 2020;21(5):517-526. doi: 10.2174/1389203720666191015145714.

Abstract

Lyme disease (LD) is an infectious disease caused by the spirochetes of genus borrelia, which are transmitted by the ticks of the genus ixodes. LD is transmitted by the spirochete B. burgdorferi sensu lato. Once in contact with the host through a tick bite, the pathogen comes into contact with the host defense, and must escape this machinery to establish LD, thus using a large number of mechanisms involving the vector of the pathogen, the pathogen itself and also the host. The initial diagnosis of the disease can be made based on the clinical symptoms of LD and the disease can be treated and cured with antibiotics if the diagnosis is made early in the beginning of the disease. Contrariwise, if LD is left untreated, the pathogen disseminates throughout the tissues and organs of the body, where it establishes different types of disease manifestations. In the nervous system, the inflammation caused by B. burgdorferi is known as Lyme neuroborreliosis (LNB). LNB is one of the principal manifestations of LD. In this review, we systematically describe the different molecular interactions among B. burgdorferi, the vector (tick) and the mammalian host.

Keywords: B. burgdorferi; Lyme borreliosis; Lyme neuroborreliosis; mammal host; molecular interaction; tick..

Publication types

  • Review

MeSH terms

  • Animals
  • Arachnid Vectors / immunology
  • Arachnid Vectors / microbiology*
  • Bacterial Proteins / genetics*
  • Bacterial Proteins / immunology
  • Borrelia burgdorferi / immunology
  • Borrelia burgdorferi / pathogenicity*
  • Cytokines / genetics
  • Cytokines / immunology
  • Gene Expression Regulation
  • Host-Pathogen Interactions / genetics*
  • Host-Pathogen Interactions / immunology
  • Humans
  • Ixodes / immunology
  • Ixodes / microbiology*
  • Lyme Disease / genetics*
  • Lyme Disease / immunology
  • Lyme Disease / microbiology
  • Lyme Disease / pathology
  • Membrane Proteins / genetics*
  • Membrane Proteins / immunology
  • Nervous System / immunology
  • Nervous System / microbiology
  • Nervous System / pathology
  • Protein Isoforms / genetics
  • Protein Isoforms / immunology
  • Receptors, Cell Surface / genetics*
  • Receptors, Cell Surface / immunology
  • Saliva / microbiology
  • Signal Transduction

Substances

  • Bacterial Proteins
  • Cytokines
  • Membrane Proteins
  • Protein Isoforms
  • Receptors, Cell Surface
  • TROSPA protein, Ixodes scapularis
  • complement regulator-acquiring surface proteins, Borrelia burgdorferi