OspA L03 Group2: Difference between revisions

Lyme disease has been affecting many individuals year around developing chronic arthritis, neurologic and cardiac abnormalities, and skin lesions (Burgdorferi, 1982). The bacterial vector, Borrelia burgdorferi is spread through the bite and feeding of ticks bringing initial severe skin lesions, erythema chronicum migrans within 10-12 weeks of infestation (Burgdorferi, 1982). Studies were first conducted through New Zealand white rabbits (Burgdorferi, 1982) through the use of indirect immunofluoresence.  

Outer surface protein A, or OspA is found to inhibit bacterial transmission <ref name=Ding >PMID: 11183781</ref>. Outer surface protein A, or OspA was found to initiate an immune response that contributed towards the development of Lyme disease vaccinations. It prevented the transmission of Borrelia burgdorferi, the causative bacterial agent of Lyme disease after the attachment of an infected tick <ref name=Ding >PMID: 11183781</ref>. Once entered the host through the skin or blood stream, Borrelia burgdorferi downregulated and suppressed OspA to minimize all of the host’s immunogenic characteristics <ref name=Ruprecht >PMID: 18097481</ref>. When OspA on the spirochete migrated to an inflammatory environment, it induced apoptosis on the bacteria through the activation of B-cells <ref name=Ruprecht >PMID: 18097481</ref>. Only OspA positive in borrelia bacteria were unable to establish an infection compared to OspA negative bacteria successfully hosted in studies of mice <ref name=Ruprecht >PMID: 18097481</ref>. OspA known as a potent stimulator of neutrophils was able to kill the pathogen and attract leukocytes allowing the release of proinflammatory cytokines in a host <ref name=Ruprecht >PMID: 18097481</ref> and avoid contracting Lyme disease as it affects the heart, joints, and nervous system <ref name=Ruprecht >PMID: 18097481</ref>.