G1SecL05: Difference between revisions
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=='''Background'''== | |||
Lyme disease, discovered in 1975<ref>PMID: 17160599</ref>, is a vector--borne disease caused by the inoculation of spirochete borrelia into the skin by members of hard bodied ticks of the family Ixodidae. Symptoms include arthritis at major joints, neurological problems such as reduced memory and poor ability to concentrate, and characteristic lesions erythema migans, more commonly known as the bull’s eye rash. A major outer surface membrane protein of Borrelia, ospA, plays a key role in immunity against Lyme disease through its binding to the antibody LA-2 fab. | |||
=='''Development of the recombinant vaccine'''== | |||
Initial approaches for vaccines to treat lyme disease solely focused on ospA after studies involving passive immunization in mice. Studies indicated that passive immunization in mice only occurred if the blood from humans infected with Lyme disease contained anti-ospA monoclonal antibodies<ref>PMID: 15864264</ref>. Although ospA vaccines, such as Lymerix, were able to halt transmission of the spirochetes, they were immediately pulled from the market due to chronic side effects such as severe arthritis. Additionally, quantitative analysis of immune response<ref>PMID:11865439</ref> of the whole ospA indicated that it is not predictive of protection. | |||
Recent developments in vaccines against Lyme Borreliosis emphasize the need to utilize the LA-2 –ospA complex on the basis that it, as a result of its specificity, induces long- term immune response in mice during previously studied clinical trials. Passive immunization of mice that resulted with significant titers of LA-2 serum antibody had a strong correlation with protection against tick transmission of infection<ref>PMID: 23407755</ref> | |||
=='''Inefficiency and concerns'''== | |||
==''' Discussion'''== | |||
<Structure load='1fj1' size='500' frame='true' align='right' caption='3D Jmol model' scene='Insert optional scene name here' /> | <Structure load='1fj1' size='500' frame='true' align='right' caption='3D Jmol model' scene='Insert optional scene name here' /> | ||
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<scene name='G1SecL05/1fj1-condensed/1'>Composite Three variable regions highlights, Tryptophan 216 - Blue, Alanine 208 - Purple, Highly Variable LA-2 Fab + OspA conjunction - Red</scene> | <scene name='G1SecL05/1fj1-condensed/1'>Composite Three variable regions highlights, Tryptophan 216 - Blue, Alanine 208 - Purple, Highly Variable LA-2 Fab + OspA conjunction - Red</scene> | ||
=='''References'''== | |||
<references /> | <references /> | ||
Revision as of 21:55, 29 April 2013
BackgroundBackground
Lyme disease, discovered in 1975[1], is a vector--borne disease caused by the inoculation of spirochete borrelia into the skin by members of hard bodied ticks of the family Ixodidae. Symptoms include arthritis at major joints, neurological problems such as reduced memory and poor ability to concentrate, and characteristic lesions erythema migans, more commonly known as the bull’s eye rash. A major outer surface membrane protein of Borrelia, ospA, plays a key role in immunity against Lyme disease through its binding to the antibody LA-2 fab.
Development of the recombinant vaccineDevelopment of the recombinant vaccine
Initial approaches for vaccines to treat lyme disease solely focused on ospA after studies involving passive immunization in mice. Studies indicated that passive immunization in mice only occurred if the blood from humans infected with Lyme disease contained anti-ospA monoclonal antibodies[2]. Although ospA vaccines, such as Lymerix, were able to halt transmission of the spirochetes, they were immediately pulled from the market due to chronic side effects such as severe arthritis. Additionally, quantitative analysis of immune response[3] of the whole ospA indicated that it is not predictive of protection.
Recent developments in vaccines against Lyme Borreliosis emphasize the need to utilize the LA-2 –ospA complex on the basis that it, as a result of its specificity, induces long- term immune response in mice during previously studied clinical trials. Passive immunization of mice that resulted with significant titers of LA-2 serum antibody had a strong correlation with protection against tick transmission of infection[4]
Inefficiency and concernsInefficiency and concerns
DiscussionDiscussion
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ReferencesReferences
- ↑ Steere AC. Lyme borreliosis in 2005, 30 years after initial observations in Lyme Connecticut. Wien Klin Wochenschr. 2006 Nov;118(21-22):625-33. PMID:17160599 doi:10.1007/s00508-006-0687-x
- ↑ Connolly SE, Benach JL. The versatile roles of antibodies in Borrelia infections. Nat Rev Microbiol. 2005 May;3(5):411-20. PMID:15864264 doi:10.1038/nrmicro1149
- ↑ Luft BJ, Dunn JJ, Lawson CL. Approaches toward the directed design of a vaccine against Borrelia burgdorferi. J Infect Dis. 2002 Feb 15;185 Suppl 1:S46-51. PMID:11865439 doi:10.1086/338463
- ↑ Embers ME, Narasimhan S. Vaccination against Lyme disease: past, present, and future. Front Cell Infect Microbiol. 2013;3:6. doi: 10.3389/fcimb.2013.00006. Epub 2013, Feb 12. PMID:23407755 doi:10.3389/fcimb.2013.00006