Abstract

The tick-transmitted bacterium Borrelia afzelii consists of a number of antigenically different strains - often defined by outer surface protein C (OspC) genotype - that coexist at stable frequencies in host populations. To investigate how host antibody responses affect strain coexistence, we measured antibody cross-reactivity to three different OspC types (OspC 2, 3 and 9) in three different strains of laboratory mice (BALB/c, C3H and C57BL/6). The extent of cross-reactivity differed between mouse strains, being higher in C3H than BALB/c and C57BL/6. In one of three pairwise comparisons of OspC types (OspC2 vs OspC9), there was evidence for asymmetry of cross-reactivity, with antibodies to OspC2 cross-reacting more strongly with OspC9 than vice versa. These results indicate that the extent of antibody-mediated competition between OspC types may depend on the composition of the host population, and that such competition may be asymmetric. We discuss the implications of these results for understanding the coexistence of OspC types.

Highlights

  • The tick-transmitted bacterium Borrelia afzelii — one of the causative agents of Lyme borreliosis in humans (Kurtenbach et al, 2006) — consists of a number of antigenically different strains (Durand et al, 2015; Hellgren et al, 2011), where the acquired immune response to one strain provides limited protection against others (Gomez-Chamorro et al, 2019; Jacquet et al, 2015)

  • To check if all mice responded to the immunization, we compared antibody levels as measured when ELISA plates were coated with the homologous outer surface protein C (OspC) with antibody levels in control mice

  • In three cases, antibody levels to heterologous OspC were barely above background levels, indicating limited crossreactivity

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Summary

Introduction

The tick-transmitted bacterium Borrelia afzelii — one of the causative agents of Lyme borreliosis in humans (Kurtenbach et al, 2006) — consists of a number of antigenically different strains (Durand et al, 2015; Hellgren et al, 2011), where the acquired immune response to one strain provides limited protection against others (Gomez-Chamorro et al, 2019; Jacquet et al, 2015). Similar patterns are observed in B. burgdorferi, another major cause of Lyme disease (Probert et al, 1997). Such antigenic diversity is common in pathogenic microbes infecting vertebrates (Lipsitch and O’Hagan, 2007). Analyses of strain fre­ quencies in populations in Sweden and Switzerland found no statisti­ cally significant change over nine and eleven years, respectively (Durand et al, 2017; Råberg et al, 2017)

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