OspA L03 Group2: Difference between revisions
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==== Pathology of OspA ==== | ==== Pathology of OspA ==== | ||
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>, while expression of OspC was active. Usually, the initial stages of Lyme disease diagnosed individuals with peaked elevations of OspC up until 7-11 weeks, then later declined (Wagner, 2012). When OspA on the spirochete migrated to an inflammatory environment, it induced [http://en.wikipedia.org/wiki/Apoptosis apoptosis] on the bacteria through the activation of [http://en.wikipedia.org/wiki/B-cells B-cells] <ref name=Ruprecht >PMID: 18097481</ref>. | Once entered the host through the skin or blood stream, Borrelia burgdorferi downregulated and suppressed OspA to minimize all of the host’s [http://en.wikipedia.org/wiki/Immunogenic immunogenic] characteristics <ref name=Ruprecht >PMID: 18097481</ref>, while expression of OspC was active. Usually, the initial stages of Lyme disease diagnosed individuals with peaked elevations of OspC up until 7-11 weeks, then later declined (Wagner, 2012). When OspA on the spirochete migrated to an inflammatory environment, it induced [http://en.wikipedia.org/wiki/Apoptosis apoptosis] on the bacteria through the activation of [http://en.wikipedia.org/wiki/B-cells B-cells] <ref name=Ruprecht >PMID: 18097481</ref>. | ||