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Caiazzo, S.

Publications and source records attributed to Caiazzo, S..

2 recordsLinked to original sources

Chemovaccination with a novel antimalarial targeting the late liver stage induces durable immunity against malaria

Vaccination with Plasmodium falciparum, the most lethal malaria parasite, using sporozoites that arrest during liver stage infection either by irradiation, genetic attenuation or chemotherapy have been developed, with late liver stage arrest providing very high efficacy. Such vaccines require complex manufacture, deployment and intravenous administration. Here, we report an alternative strategy of chemo-attenuation of malaria parasites at the late liver stage using first-in-class antimalarials under clinical development that target the parasite aspartyl proteases plasmepsin IX and X. A single low-dose infection with virulent Plasmodium berghei sporozoites followed by drug treatment cleared infection by producing chemo-attenuated liver merozoites (CALM) that induced sterile immunity in mice for up to 21 months. Protection arose from humoral responses to circumsporozoite protein and robust CD8+ T cell responses, including liver-resident memory cells reactive to diverse antigens including SERA1 and RPL6. Drug treatment also attenuated the human pathogen P. falciparum by preventing liver merozoites from infecting human erythrocytes in humanized chimeric liver mice, confirming that the mechanism of liver-stage merozoite attenuation (ie, CALM) via inhibition of plasmepsins IX and X is conserved, likely due to conservation of binding site amino acids of both proteases across the Plasmodium genus. Therefore, plasmepsin IX/X-targeting antimalarials offer a new approach to achieving late liver stage arrest against all circulating Plasmodium species and strains. This study establishes the basis for clinical trials assessing CALM for chemoprevention and chemovaccination against diverse Plasmodium species to advance new therapeutic strategies in malaria control. It also suggests the prospect of chemovaccination by natural exposure to mosquito-borne parasites if development of a long-acting injectable formulation of plasmepsin IX/X inhibitors proves feasible.

microbiology↗

Host iron deficiency protects against Plasmodium infection and drives parasite molecular reprofiling.

Iron deficiency, anemia and Plasmodium infection represent significant global health challenges with overlapping geographical distributions, particularly affecting pregnant women in Africa, yet the mechanisms underlying their interactions remain poorly understood. We employed a multilayered approach combining clinical data from Malawian pregnant women (n=711) in the REVAMP trial, a genetic mouse model (Tmprss6-knockout), and in vitro P. falciparum cultures to clarify associations between iron status and malaria susceptibility. Iron deficiency was associated with 50% reduced P. falciparum parasitemia in pregnant women (95% CI [30%-64%], p<0.0001), while iron-deficient mice exhibited significantly improved survival against P. berghei (median 15.5 days vs. 7.0 days for WT mice) and protection from cerebral malaria (83% vs 17% survival). Iron chelation induced substantial transcriptomic and proteomic changes in cultured parasites, affecting host cell invasion and nutrient acquisition processes. Importantly, intravenous iron supplementation did not increase subsequent parasitemia when coupled with malaria prevention. These findings demonstrate that iron deficiency protects against Plasmodium infection and support WHO recommendations for iron supplementation in malaria-endemic regions when combined with adequate malaria prevention strategies.

cell biology↗