Duration of immunity to reinfection with tick-transmitted Borrelia burgdorferi in naturally infected mice

Piesman, Joseph; Dolan, Marc C.; Happ, Christine M.; Luft, Benjamin J.; Rooney, Sean; Mather, Thomas N.; Golde, William T.

doi:10.1128/iai.65.10.4043-4047.1997

Cited by 37 publications

(18 citation statements)

References 25 publications

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“…It was previously shown that active infection followed by antibiotic treatment and then challenge with infected-tissue transplants prevents homologous transplantborne infection (4). Likewise, a recently published study demonstrated that active infection followed by antibiotic treatment protects mice against tick-borne challenge infection with the same B. burgdorferi strain for over 1 year (39). This result is in keeping with my findings of durable (1-year) protective immunity against homologous challenge with cultured spirochetes, regardless of challenge dose (up to 10 6 spirochetes), and protective immunity against homologous transplant-borne challenge.…”

Section: Discussionsupporting

confidence: 82%

Specificity of Infection-Induced Immunity amongBorrelia burgdorferiSensu Lato Species

Barthold

1999

Infect Immun

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The specificity of infection-induced immunity in mice infected with cultured or host-adapted Borrelia burgdorferi sensu lato, the agent of Lyme disease, was examined. Sera obtained from mice following infection with high and low doses of cultured B. burgdorferi sensu stricto, transplantation of infected tissue (host-adapted spirochetes), or tick-borne inoculation all showed protective activity in passive immunization assays. Infection and disease were similar in mice infected with cultured spirochetes or by transplantation. Thus, the adaptive form of inoculated spirochetes did not influence the immune response during active infection. Mice infected with B. burgdorferi sensu stricto and then cured of infection with an antibiotic during early or late stages of infection were resistant to challenge with high doses of homologous cultured spirochetes for up to 1 year. In contrast, actively immune mice infected with different Borrelia species (B. burgdorferi sensu lato, B. burgdorferi sensu stricto cN40, Borrelia afzelii PKo, and Borrelia garinii PBi) and then treated with an antibiotic were resistant to challenge with cultured homologous but not heterologous spirochetes. Similar results were achieved for actively immune mice challenged by transplantation and by passive immunization with sera from mice infected with each of the Borrelia species and then challenged with cultured spirochetes. Arthritis and carditis in mice that had immunizing infections with B. afzelii and B. garinii and then challenged by transplantation with B. burgdorferi sensu stricto were equivalent in prevalence and severity to those in nonimmune recipient mice. These results indicate that protective immunity and disease-modulating immunity that develop during active infection are universal among species related to B. burgdorferi sensu lato but are species specific.

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Section: Discussionsupporting

confidence: 82%

Specificity of Infection-Induced Immunity amongBorrelia burgdorferiSensu Lato Species

Barthold

1999

Infect Immun

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“…The absolute requirement for the vls locus in persistence associated with Lyme disease led us to question whether mice originally infected with spirochetes lacking VlsE could be reinfected with a fully infectious clone that has an intact vls recombination system. Previous studies have shown that cured mice are immune to reinfection when challenged by intradermal inoculation or with an autograft from infected mice (Barthold, 1993;Piesman et al, 1997). However, these studies involved challenging actively immunized mice previously infected with a fully infectious clone of B. burgdorferi with autologous isolates, compared with the present study, where mice naturally cleared of partially infectious spirochetes are challenged with fully infectious clones.…”

Section: Vlse Does Not Appear To Confer Reinfection Abilitymentioning

confidence: 91%

The role of VlsE antigenic variation in the Lyme disease spirochete: persistence through a mechanism that differs from other pathogens

Bankhead

Chaconas²

2007

Molecular Microbiology

148

198

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SummaryThe linear plasmid, lp28-1, is required for persistent infection by the Lyme disease spirochete, Borrelia burgdorferi. This plasmid contains the vls antigenic variation locus, which has long been thought to be important for immune evasion. However, the role of the vls locus as a virulence factor during mammalian infection has not been clearly defined. We report the successful removal of the vls locus through telomere resolvase-mediated targeted deletion, and demonstrate the absolute requirement of this lp28-1 component for persistence in the mouse host. Moreover, successful infection of C3H/HeN mice with an lp28-1 plasmid in which the left portion was deleted excludes participation of other lp28-1 non-vls genes in spirochete virulence, persistence and the process of recombinational switching at vlsE. Data are also presented that cast doubt on an immune evasion mechanism whereby VlsE directly masks other surface antigens similar to what has been observed for several other pathogens that undergo recombinational antigenic variation.

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“…Acquired immunity in the vertebrate host plays an important role in the epidemiology of Lyme disease (Johnson et al ., 1986a,b; Kurtenbach et al ., ; Piesman et al ., ; Liang et al ., ). One Borrelia antigen that is particularly important for the pathogen's interaction with the vertebrate immune system is outer surface protein C (OspC) (Radolf and Caimano, ).…”

Section: Introductionmentioning

confidence: 99%

Strain‐specific antibodies reduce co‐feeding transmission of the Lyme disease pathogen, Borrelia afzelii

Jacquet

Durand

Rais

et al. 2015

Environmental Microbiology

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Vector-borne pathogens use a diversity of strategies to evade the vertebrate immune system. Co-feeding transmission is a potential immune evasion strategy because the vector-borne pathogen minimizes the time spent in the vertebrate host. We tested whether the Lyme disease pathogen, Borrelia afzelii, can use co-feeding transmission to escape the acquired immune response in the vertebrate host. We induced a strain-specific, protective antibody response by immunizing mice with one of two variants of OspC (A3 and A10), the highly variable outer surface protein C of Borrelia pathogens. Immunized mice were challenged via tick bite with B. afzelii strains A3 or A10 and infested with larval ticks at days 2 and 34 post-infection to measure co-feeding and systemic transmission respectively. Antibodies against a particular OspC variant significantly reduced co-feeding transmission of the targeted (homologous) strain but not the non-targeted (heterologous) strain. Cross-immunity between OspC antigens had no effect in co-feeding ticks but reduced the spirochaete load twofold in ticks infected via systemic transmission. In summary, OspC-specific antibodies reduced co-feeding transmission of a homologous but not a heterologous strain of B. afzelii. Co-feeding transmission allowed B. afzelii to evade the negative consequences of cross-immunity on the tick spirochaete load.

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Duration of immunity to reinfection with tick-transmitted Borrelia burgdorferi in naturally infected mice

Cited by 37 publications

References 25 publications

Specificity of Infection-Induced Immunity amongBorrelia burgdorferiSensu Lato Species

Specificity of Infection-Induced Immunity amongBorrelia burgdorferiSensu Lato Species

The role of VlsE antigenic variation in the Lyme disease spirochete: persistence through a mechanism that differs from other pathogens

Strain‐specific antibodies reduce co‐feeding transmission of the Lyme disease pathogen, Borrelia afzelii

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