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Inactivation of Genes for Antigenic Variation in the Relapsing Fever Spirochete Reduces Infectivity in Mice and Transmission by Ticks
Borrelia hermsii, an agent of tick-borne relapsing fever when infecting humans, employs antigenic variation of the variable major proteins (Vmps) to escape the host immune response. This mechanism allows the bacteria to persist in the blood of a mammal, which increases their potential for acquisition by their tick vector Ornithodoros hermsi. Once in the tick, the bacteria move from the midgut to salivary glands where the Vmps are replaced with another major surface protein, the variable tick protein (Vtp). We constructed two mutants, one that was unable to produce a Vmp (Vmp−) and another that was unable to produce Vtp (Δvtp). The Vmp − mutant could not reach as high bacterial levels in the blood of mice when infected by needle-inoculation and tick bite compared to the parent strain, and was incapable of relapsing. The Δvtp mutant was able to colonize ticks, but was non-infectious by tick bite. Our study provides insight into the roles of the Vmps and Vtp in the infectivity of B. hermsii by showing the importance of antigenic variation for prolonging bacteria levels in the host as well as the requirement of Vtp for mammalian infection by the bite of its tick vector.
Vyšlo v časopise: Inactivation of Genes for Antigenic Variation in the Relapsing Fever Spirochete Reduces Infectivity in Mice and Transmission by Ticks. PLoS Pathog 10(4): e32767. doi:10.1371/journal.ppat.1004056
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004056Souhrn
Borrelia hermsii, an agent of tick-borne relapsing fever when infecting humans, employs antigenic variation of the variable major proteins (Vmps) to escape the host immune response. This mechanism allows the bacteria to persist in the blood of a mammal, which increases their potential for acquisition by their tick vector Ornithodoros hermsi. Once in the tick, the bacteria move from the midgut to salivary glands where the Vmps are replaced with another major surface protein, the variable tick protein (Vtp). We constructed two mutants, one that was unable to produce a Vmp (Vmp−) and another that was unable to produce Vtp (Δvtp). The Vmp − mutant could not reach as high bacterial levels in the blood of mice when infected by needle-inoculation and tick bite compared to the parent strain, and was incapable of relapsing. The Δvtp mutant was able to colonize ticks, but was non-infectious by tick bite. Our study provides insight into the roles of the Vmps and Vtp in the infectivity of B. hermsii by showing the importance of antigenic variation for prolonging bacteria levels in the host as well as the requirement of Vtp for mammalian infection by the bite of its tick vector.
Zdroje
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