AP2-L-Dependent Processes Promote PVM Maintenance and Plasmodium Liver-stage Development

Deleting P. berghei ap2-l prevents sporozoite establishment of blood-stage infection in mice and disrupts liver-stage development, with reduced EEF numbers and sizes.

• Why it matters: Malaria depends on sporozoites forming replicative exo-erythrocytic forms inside hepatocytes, requiring a functional PVM and host interactions, but AP2-L’s role in these steps is unclear.
• What they did: The study generated an ap2-l knockout and assessed erythrocytic replication in vivo, sporozoite gene expression, liver-stage development in infected HepG2 cells, and PVM protein localization and detergent sensitivity.
• The result: AP2-L loss lowered transcripts for motility, entry, and rhoptry secretion, caused aberrant PVM organization with missing tubular extensions, reduced parasite DNA replication, and increased host autophagy protein accumulation around parasites.

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