Complement evasion by apicomplexans: Convergent strategies across diverse parasites

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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Publication Details

Journal
PLoS Pathogens
Published
2026-07-17
DOI
https://doi.org/10.1371/journal.ppat.1014435
Primary Topic
Complement system in diseases
Type
article
Field-Weighted Citation Impact
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article

Complement evasion by apicomplexans: Convergent strategies across diverse parasites

Carlos J. Ramírez‐Flores, Sofía Espinosa-Hernández
PLoS Pathogens
Complement system in diseases
article

Complement evasion by apicomplexans: Convergent strategies across diverse parasites

Carlos J. Ramírez‐Flores, Sofía Espinosa-Hernández
article en

Abstract

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.

PLoS PathogensVol. 22(7)
Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (MX)
Openalex Percentile: Top 14%
Complement system in diseases
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