User:Marvin O'Neal/OspC: Difference between revisions

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{{STRUCTURE_1ggq| PDB=1ggq | SCENE=Studio:G4SecL04/Initial_02/1}}
{{STRUCTURE_1ggq| PDB=1ggq | SCENE=Studio:G4SecL04/Initial_02/1}}
Lyme disease is a typical epidemic in northeastern and north central regions of the United States. It is also the most prevalent tick-borne disease which is caused by ''Borrelia burgdoferi'',a spirochete that is identified in ''Ixodes scapulars''. Humans infected with Lyme disease begin with unusal skin lesions (erythema chronicum migrans), which later develop into more severe neurological and cardiac symptoms
 
<ref>PMID:7043737</ref>. If it is not completely treated, the causative agent of Lyme disease persists in human by interacting the surface-exposed ''B. burgdoferi'' proteins with the molecules of the host. Among 100 different lipoproteins present in its outer surface, the outer surface protein C (OspC) is one of its major host-induced antigens, but is inactive due to the immune response of mammalian host during its early age. The expression of OspC is dependent on temperature and it is induced when the tick migrates from guts to salivary gland during feeding period. OspC is highly polymorphic that based on alignment sequence, its genetic diversity at the OspC locus that can be categorized into 19 outer surface protein major groups (oMGs) ranged from type A to S. However, only four invasive allelic groups: A, B, I([[1f1m]]), and K, are responsible for causing human Lyme disease.
Lyme disease is caused by "Borrelia burgdoferi", a spirochete that is identified in "Ixodes scapulars". It is the most prevalent tick-borne disease in North America and Europe. Humans infected with Lyme disease begin with unusal skin lesions (erythema migrans), which later develop into more severe neurological and cardiac symptoms if it is not treated<ref>PMID:7043737</ref>. Thus, "B. burgdoferi" persists in human by interacting its surface-exposed proteins with the molecules of the host. This interaction of its outer surface proteins (Osps) is very crucial for the pathogenic pathway of Lyme disease. When the ticks bite on human, "B. burgodoferi" in the unfed ticks, which colonize in the midgut, produces OspA, OspB but no OspC. However, the tick migrates from guts to salivary gland during feeding period, OspC is upregulated, thereby inducing OspC synthesis and inhibiting the expression of OspA and OspB due to changes in environmental temperature and pH. Therefore, the vaccine against Lyme disease named OspA-based LYMErix vaccine was available for human use from 1998 to 2002. However, it was withdrawn because of its vaccine-associated autoimmune risk factors. In addition, the majority of ticks reside in the tick silva do not have OspA, but OspC is present during the early infection. Nowadays, scientists are trying to find new OspC-based vaccine as an effective target of immunity. Even though OspC has stable antigenic site on its outer surface during infection, the vaccine of recombinant anti-OspC are effective only for the spirochetes with identical sequence of OspC because OspC is a highly variable protein. Its genetic diversity at OspC locus can be categroized into 19 outer surface major groups (oMGs), denoted by type A to S. Based on its alignment sequence, the sequence variation within a major group is 1% whereas approximately 15% between major groups. However, only four invasive allelic groups: A, B, I([[1f1m]]), and K, are responsible for causing human Lyme disease. Therefore, polymorphism of OspC driven by the ecological interaction in natural "B. burgdoferi" plays an essential role in discovering anti-OspC based vaccine to prevent the prevalence and risk of human Lyme disease. 


== Ecology of Lyme Disease ==
== Ecology of Lyme Disease ==