This analysis defines mechanisms of complement evasion in apicomplexan parasites, suggesting critical survival adaptations.
Apicomplexan parasites encounter the complement system during extracellular stages of infection, where it imposes a major barrier to survival. Complement activation promotes pathogen elimination through opsonization, inflammation, and membrane attack complex (MAC) formation. To persist, apicomplexans deploy mechanistically distinct but functionally convergent strategies that modulate complement activity instead of fully inhibiting it. These include rapid invasion to limit extracellular exposure, recruitment of host complement regulatory proteins, surface shielding to prevent MAC insertion, and direct interference with complement activation. A central feature of these strategies is the regulation of C3 deposition and processing, which determines downstream effector outcomes. Here, we define a unifying framework for complement evasion across apicomplexans based on these four mechanisms.
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Espinosa-Hernández et al. (2026) studied this question.
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