Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F21%3A43903627" target="_blank" >RIV/60076658:12310/21:43903627 - isvavai.cz</a>

Alternative codes found

RIV/60077344:_____/21:00553232

Result on the web

<a href="https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009801" target="_blank" >https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009801</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1371/journal.ppat.1009801" target="_blank" >10.1371/journal.ppat.1009801</a>

Result language

angličtina

Original language name

Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system

Original language description

Pathogens possess the ability to adapt and survive in some host species but not in others-an ecological trait known as host tropism. Transmitted through ticks and carried mainly by mammals and birds, the Lyme disease (LD) bacterium is a well-suited model to study such tropism. Three main causative agents of LD, Borrelia burgdorferi, B. afzelii, and B. garinii, vary in host ranges through mechanisms eluding characterization. By feeding ticks infected with different Borrelia species, utilizing feeding chambers and live mice and quail, we found species-level differences in bacterial transmission. These differences localize on the tick blood meal, and specifically complement, a defense in vertebrate blood, and a polymorphic bacterial protein, CspA, which inactivates complement by binding to a host complement inhibitor, Factor H (FH). CspA selectively confers bacterial transmission to vertebrates that produce FH capable of allele-specific recognition. CspA is the only member of the Pfam54 gene family to exhibit host-specific FH-binding. Phylogenetic analyses revealed convergent evolution as the driver of such uniqueness, and that FH-binding likely emerged during the last glacial maximum. Our results identify a determinant of host tropism in Lyme disease infection, thus defining an evolutionary mechanism that shapes host-pathogen associations. Author summary The evolution of pathogens in response to a host environment often leads to a specificity of these pathogens to survive in particular hosts, known as host tropism. However, the mechanisms of host tropism remain unclear. The Lyme disease (LD) bacterium is an ideal model to study such mechanisms because the causative agent of this disease (bacteria species) are transmitted by ticks and carried by multiple vertebrates, including mammals and birds. We found that different LD bacteria species vary in their ability to survive in mice and quail, and in ticks fed on human or quail blood after transmission. We also showed that such a variation is dependent on whether tick blood meals have functional complement, an innate defense in vertebrate blood. We attributed such species-to-species differences of transmission to the polymorphisms of a bacterial complement inactivating protein, CspA: CspA, by inactivating vertebrate complement in tick blood meals in a species-specific manner, allows bacterial transmission to selective vertebrates. We further demonstrated that this CspA-mediated bacterium species-specific complement evasion arose through convergent evolution, as an evolutionary mechanism to permit such vertebrate-bacteria interaction. The mechanisms defined in this multi-disciplinary work provide new insights into the host-pathogen interactions.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

10608 - Biochemistry and molecular biology

Project

<a href="/en/project/GA17-21244S" target="_blank" >GA17-21244S: Delineating the role of Borreli afzelii genes required for dissemination within an infected tick during feeding</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2021

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

PLoS Pathogens

ISSN

1553-7366

e-ISSN

—

Volume of the periodical

17

Issue of the periodical within the volume

7

Country of publishing house

US - UNITED STATES

Number of pages

29

Pages from-to

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UT code for WoS article

000685216800009

EID of the result in the Scopus database

2-s2.0-85111499152