Strategies for Recombination and Variation of Bacterial Antigens

Introduction The survival of a pathogen requires the evasion of host immunity, either through switching hosts, utilizing a life history strategy allowing the pathogen to be free-living some of the time, finding sites within a host that are “privileged” or hidden from host immunity, or switching the composition of an antigen. Pathogens interact with hosts through antigens, typically proteins expressed on a cell surface and commonly inciting some immune response by the host. Varying antigen structure has evolved independently multiple times across kingdoms and phyla of eukaryotes and prokaryotes, reaching particular importance in obligately parasitic organisms that cause chronic infection in hosts. For example, because vector-borne and sexually transmitted pathogens often rely for survival on infection that persists long enough for a new vector or host to acquire the infection, chronic infection and antigenic variation are common in these pathogens (Palmer et al. 2009). Mechanisms of production of variant antigen genes vary in specifics, but for most eukaryotes and prokaryotes (in contrast with viruses, which often utilize point mutations), larger scale variation is the rule, accomplished through recombination (Palmer et al. 2009). There are epigenetic, transcriptional, and translational regulatory mechanisms for varying antigens as well, which are outside the scope of the present paper. This review will describe a suite of prokaryotic pathogens that vary antigens most likely to evade host immunity and promote chronic infection, describe mechanisms for production of variants, and synthesize evolutionary forces and constraints that shape the coevolutionary phenomenon of antigenic variation among diverse bacterial genera.