Sickle cell trait (HbAS genotype) confers resistance to severe falciparum malaria. The mechanism involves:

• A HbS reduces Duffy antigen expression needed for P. falciparum invasion
• B Increased 2,3-BPG in HbAS cells kills intraerythrocytic trophozoites
• C HbS activates complement-mediated lysis of merozoites
• D Sickling of infected RBCs at low O2 tension in microvasculature causes premature phagocytic clearance of parasites ✓

Explanation

In low-O2 microvascular environments (e.g., spleen, infected capillaries), HbAS RBCs can sickle sufficiently to trigger premature phagocytic recognition and removal before parasite maturation — presenting 'non-functional' Hb to the parasite and restricting intracellular replication. Additionally, parasitized HbAS cells display altered surface antigens, improving immune recognition. Duffy antigen (FY) is used by P. vivax for invasion. 2,3-BPG modulates O2 affinity but is not directly parasitocidal. Complement-mediated killing of merozoites is not the primary protective mechanism.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.