New Zealand white rabbits effectively clear borrelia burgdorferi B31 despite the bacterium's functional vlse antigenic variation system
Batool M., Hillhouse A. E., Ionov Y., Kochan K. J., Mohebbi F., Stoica G., Threadgill D. W., Zelikovskij A. Z., Waghela S. D., Wiener D. J., Rogovskyy A. S.
Infection and Immunity
Vol.87, Issue7, Num.e00164-19
Опубликовано: 2019
Тип ресурса: Статья
Аннотация:
Borrelia burgdorferi is a tick-borne bacterium responsible for approximately 300,000 annual cases of Lyme disease (LD) in the United States, with increasing incidences in other parts of the world. The debilitating nature of LD is mainly attributed to the ability of B. burgdorferi to persist in patients for many years despite strong anti-Borrelia antibody responses. Antimicrobial treatment of persistent infection is challenging. Similar to infection of humans, B. burgdorferi establishes long-term infection in various experimental animal models except for New Zealand White (NZW) rabbits, which clear the spirochete within 4 to 12 weeks. LD spirochetes have a highly evolved antigenic variation vls system, on the lp28-1 plasmid, where gene conversion results in surface expression of the antigenically variable VlsE protein. VlsE is required for B. burgdorferi to establish persistent infection by continually evading otherwise potent antibodies. Since the clearance of B. burgdorferi is mediate
Ключевые слова:
Antigenic variation; Borrelia burgdorferi; Immune evasion; Lyme disease; Persistent infection; VlsE
rabbit antiserum; bacterial antigen; bacterial protein; bacterium antibody; lipoprotein; animal experiment; animal model; animal tissue; antibody response; antigenic variation; arthritis; Article; bacterial clearance; Borrelia burgdorferi; complement activation; controlled study; cross protection; erythema chronicum migrans; exudate; gene conversion; gene expression; heart tissue; histopathology; humoral immunity; immune evasion; in vitro study; Lyme disease; male; mouse; nonhuman; osteolysis; passive immunization; persistent infection; priority journal; rabbit model; RecA gene; skin biopsy; tibiotarsal joint; animal; antigenic variation; Borrelia burgdorferi; genetics; immunology; Leporidae; Lyme disease; microbiology; physiology; plasmid; Animals; Antibodies, Bacterial; Antigenic Variation; Antigens, Bacterial; Bacterial Proteins; Borrelia burgdorferi; Lipoproteins; Lyme Disease; Plasmids; Rabbits
Язык текста: Английский
ISSN: 1098-5522
Batool M.
Hillhouse A. E.
Ionov Y.
Kochan K. J.
Mohebbi F.
Stoica G.
Threadgill D. W.
Zelikovskij A. Z. Aleksandr Zinovij 1960-
Waghela S. D.
Wiener D. J.
Rogovskyy A. S.
Батоол М.
Хиллхоусе А. Е.
Ионов Y.
Кочан К. Й.
Мохебби Ф.
Стоиcа Г.
Тхреадгилл Д. W.
Зеликовский А. З. Александр Зиновий 1960-
Wагхела С. Д.
Wиенер Д. Й.
Роговскyy А. С.
New Zealand white rabbits effectively clear borrelia burgdorferi B31 despite the bacterium's functional vlse antigenic variation system
Текст визуальный непосредственный
Infection and Immunity
American Society for Microbiology
Vol.87, Issue7 Num.e00164-19
2019
Статья
Antigenic variation Borrelia burgdorferi Immune evasion Lyme disease Persistent infection VlsE
rabbit antiserum bacterial antigen bacterial protein bacterium antibody lipoprotein animal experiment animal model animal tissue antibody response antigenic variation arthritis Article bacterial clearance Borrelia burgdorferi complement activation controlled study cross protection erythema chronicum migrans exudate gene conversion gene expression heart tissue histopathology humoral immunity immune evasion in vitro study Lyme disease male mouse nonhuman osteolysis passive immunization persistent infection priority journal rabbit model RecA gene skin biopsy tibiotarsal joint animal antigenic variation Borrelia burgdorferi genetics immunology Leporidae Lyme disease microbiology physiology plasmid Animals Antibodies, Bacterial Antigenic Variation Antigens, Bacterial Bacterial Proteins Borrelia burgdorferi Lipoproteins Lyme Disease Plasmids Rabbits
Borrelia burgdorferi is a tick-borne bacterium responsible for approximately 300,000 annual cases of Lyme disease (LD) in the United States, with increasing incidences in other parts of the world. The debilitating nature of LD is mainly attributed to the ability of B. burgdorferi to persist in patients for many years despite strong anti-Borrelia antibody responses. Antimicrobial treatment of persistent infection is challenging. Similar to infection of humans, B. burgdorferi establishes long-term infection in various experimental animal models except for New Zealand White (NZW) rabbits, which clear the spirochete within 4 to 12 weeks. LD spirochetes have a highly evolved antigenic variation vls system, on the lp28-1 plasmid, where gene conversion results in surface expression of the antigenically variable VlsE protein. VlsE is required for B. burgdorferi to establish persistent infection by continually evading otherwise potent antibodies. Since the clearance of B. burgdorferi is mediate