PT  - JOURNAL ARTICLE
AU  - Thomas M. Hart
AU  - Alan P. Dupuis II
AU  - Danielle M. Tufts
AU  - Anna M. Blom
AU  - Simon Starkey
AU  - Ryan O. M. Rego
AU  - Sanjay Ram
AU  - Peter Kraiczy
AU  - Laura D. Kramer
AU  - Maria A. Diuk-Wasser
AU  - Sergios-Orestis Kolokotronis
AU  - Yi-Pin Lin
TI  - Host tropism determination by convergent evolution of immunological evasion in the Lyme disease system
AID  - 10.1101/2021.02.09.430532
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.02.09.430532
4099  - http://biorxiv.org/content/early/2021/02/10/2021.02.09.430532.short
4100  - http://biorxiv.org/content/early/2021/02/10/2021.02.09.430532.full
AB  - Microparasites selectively adapt in some hosts, 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. LD bacteria species vary in host ranges through mechanisms eluding characterization. By feeding ticks infected with different LD bacteria species, utilizing feeding chambers and live mice and quail, we found species-level differences of bacterial transmission. These differences localize on the tick blood meal, and complement, a defense in vertebrate blood, and a bacterial polymorphic protein, CspA, which inactivates complement by binding to a host complement inhibitor, FH. CspA selectively confers bacterial transmission to vertebrates that produce FH capable of allele-specific recognition. Phylogenetic analyses revealed convergent evolution as the driver of such findings, which likely emerged during the last glacial maximum. Our results identify LD bacterial determinants of host tropism, defining an evolutionary mechanism that shapes host-microparasite associations.Competing Interest StatementThe authors have declared no competing interest.