OspA L03 Group2: Difference between revisions
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=='''Introduction'''== | =='''Introduction'''== | ||
Lyme disease has been effecting many individuals year round 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 allowing sever skin lesions to errupt and within 10-12 weeks of infestation, erythema chronicum migrans appear as well(Burgdorferi, 1982). Studies were first conducted through New Zealand white rabbits (Burgdorferi, 1982) through the use of indirect immunofluoresence. | Lyme disease has been effecting many individuals year round 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 allowing sever skin lesions to errupt and within 10-12 weeks of infestation, erythema chronicum migrans appear as well(Burgdorferi, 1982). Studies were first conducted through New Zealand white rabbits (Burgdorferi, 1982) through the use of indirect immunofluoresence. | ||
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=='''About OspA'''== | =='''About OspA'''== | ||
OspA is a lipoprotein found on the outer surface of the bacteria that is found to inhibit bacterial transmission <ref name=Ding >PMID: 11183781</ref>. In order for Lyme Disease to start and progress in the human or animal body, the initial levels of OspA is underregulated, inactivated, hidden, or OspA negative <ref name=Ding >PMID: 11183781</ref>. The bacteria underregulates OspA for the reason that it does not want to trigger any innate immune response from the host <ref name=Ding >PMID: 11183781</ref>. Experiments that showed the success of the Borrelia bacteria progressing in the body, were done through mice. Only OspA- positive borrelia admitted to apoptosis in the host; therefore, when the outer surface protein was present the Borrelia bacteria cannot survive <ref name=Ding >PMID: 11183781</ref>. Unless the vaccine with OspA is administered, or the bacteria has moved to a different environment of the cerebrospinal fluid or an inflammatory environment, the bacteria will activate and start to regulate OspA <ref name=Ding >PMID: 11183781</ref> by activating B-cells. Later this induced astrogliosis. | |||
The whole system of OspA on the antigen interacting with the antibodies was a cascade complement system. Once the complement found OspA on borrelia, it induced an innate response of phagocytosis. Not only did OspA allowed opsonization, but also attracted leukocytes (<ref name=Ding >PMID: 11183781</ref>. | |||
=='''Structure'''== | =='''Structure'''== | ||
