Most relapsing fever bacteria that infect humans are spread by ticks, but Borrelia recurrentis is unique in being transmitted between humans via body lice. Now, new genomic evidence from ancient British remains suggests that B. recurrentis diverged from its tick-borne relatives and began adapting to transmission by lice between 6000 and 4000 years ago – coinciding with the widespread use of wool textiles by humans. The findings underscore how ancient DNA can illuminate the origins and evolution of infectious diseases and how pathogens like B. recurrentis have been shaped by human social transformations. Several pathogenic bacterial species that once relied on ticks for transmission have independently evolved to use lice as vectors instead, including B. recurrentis. B. recurrentis has no known animal reservoir. Moreover, this louse-adapted pathogen tends to show higher virulence compared to its tick-borne relatives, suggesting a process of specialization. However, the precise timeline and genetic mechanisms behind its adaptation to lice and its increased virulence in humans remain uncertain.
Using advanced ancient DNA techniques optimized for degraded genetic material, Pooja Swali and colleagues recovered and analyzed four ancient B. recurrentis genomes from human remains in Britain, dating from roughly 2300 to 600 years ago. Through phylogenetic and pan-genome analysis, Swali et al. estimate that B. recurrentis diverged from its closest relative, B. duttonii, approximately 4700 – 5600 years ago. This period coincided with shifts in human behavior during the Neolithic-Bronze Age transition, such as the rise of sedentary lifestyles, the advent of wool textiles, and densely populated settlements. According to the authors, these changes may have facilitated the adaptation of B. recurrentis to the human body louse and also promoted genome reduction and host specialization. Over time, B. recurrentis underwent substantial genome reductions, particularly in plasmid-encoded genes. These genetic changes were accompanied by gains and losses of surface proteins that help the bacterium evade the host immune system.
