Abstract
The interactions between avian mycoplasmas and their host cells are far more complex than might be anticipated from their apparent structural and functional simplicity. Phenotypic diversity in the form of reversible phase variation, antigenic variation or size variation is an adaptive mechanism that enables avian mycoplasmas to survive in a hostile and highly evolved host. Despite significant similarities between major membrane antigens of Mycoplasma gallisepticum and Mycoplasma synoviae, the molecular mechanisms that mediate phenotypic variation in these two pathogens are completely different. Throughout the years, these mechanisms have evolved side by side with their host immune system and provided mycoplasmas the capacity to colonize, invade and persist in an intricate host. In this article, recent advances in the understanding of the molecular mechanisms of phenotypic variation are reviewed, and implications of such variation in pathogenesis of the disease and development of vaccines and diagnostic assays are outlined.
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