Lyme disease is an infectious neurological disease caused by a tick. Ticks are invertebrate organisms containing an external skeleton and are commonly referred to as arthropods. When ticks feed on the human host, they release a number of substances locally; anticoagulants (compounds that prevent blood clotting), vasodilators (compounds that increase the diameter of blood vessels) and substances that dampen the body’s immune response. This local release allows for the tick to evade the host’s initial immune defenses, helping the tick remain on the human host for extended periods of time. A tick must remain attached to a human host for between 36 to 48 hours in order to cause disease induction. In the case of Lyme disease, bacteria of the genus Borrelia, which live in the gut of the tick, are released into the bloodstream.
Often, individuals infected with Lyme disease may experience non-specific symptoms, which delays or prevents them from seeking medical attention. These vague, “common” symptoms that occur in many conditions include joint pain, rash, headache and flu-like symptoms and make diagnosing Lyme disease difficult. Prolonged, untreated Lyme disease may result in an individual losing the ability to read, write and communicate. Understanding the genetics of the tick vector (Ixodes scapularis) will likely provide insight into their capacity to be Borrelia carriers and potentially, therapeutic targets.
Gulia-Nuss and colleagues found that the I. scapularis genome contains 28 chromosomes. Further genetic analysis revealed that these 28 chromosomes are highly repetitive in the central region. Interestingly, approximately 60% of I. scapularis DNA is practically identical to the DNA of its other arthropod “family members”. Other arthropods have been studied extensively. Therapies aimed at targeting these other arthropods may be useful for the treatment of Lyme disease patients.
Gulia-Nuss et al. also conducted a protein screen of both early and late I. scapularis infections. Eighty-three proteins were differentially expressed between the two populations; 33 being overexpressed and 50 being under-expressed. The altered expression of these proteins resulted in aberrant β-tubulin levels, Na+/K+ ATPase expression and fatty-acid binding protein concentration. All three of these proteins are important for normal neurologic function, maintenance and stability. Restoring normal levels of the three proteins listed above may repair the neurologic state of Lyme disease patients. One treatment for resolving abnormal levels of the Na+/K+ ATPase and fatty-acid binding protein is increasing antioxidant consumption. The overarching question from this research is, do antioxidants (and changes in diet) hold the key for treating Lyme disease patients?
 Gulia-Nuss, M., Nuss, A. B., Meyer, J. M., Sonenshine, D. E., Roe, R. M., Waterhouse, R. M., . . Hill, C. A. (2016). Genomic insights into the ixodes scapularis tick vector of lyme disease. Nature Communications, 7doi:10.1038/ncomms10507