Plasmodium knowlesi Adapts In Vitro to Infect Duffy-Negative Erythrocytes

Plasmodium knowlesi, a parasite traditionally found in long-tailed macaques, has emerged as a significant cause of human malaria across Southeast Asia [1]. For decades, clinical susceptibility to this species and its close relative, Plasmodium vivax, was believed to be restricted to individuals expressing the Duffy-Antigen Receptor for Chemokine on their red blood cells [2, 3]. This genetic requirement has historically protected Duffy-negative populations, particularly those of African descent, from clinical infection [4, 5]. However, as other human malaria species face elimination, the rising incidence of P. knowlesi suggests an increasing capacity for this zoonotic pathogen to cross host species barriers [6, 7]. A recent study offers fresh insights into the molecular mechanisms that allow this parasite to overcome established host resistance factors, raising concerns about its potential to spread into new, previously protected patient populations.