Plasmodium vivax infects hepatocytes to form schizonts that cause blood infection, or dormant hypnozoites that can persist for months in the liver before leading to relapsing blood infections. The molecular processes that drive P. vivax schizont and hypnozoite survival remain largely unknown, but they likely involve a rich network of host-pathogen interactions, including those occurring at the host-parasite interface, the parasitophorous vacuole membrane (PVM). Using a recently developed P. vivax liver-stage model system we demonstrate that host aquaporin-3 (AQP3) localizes to the PVM of schizonts and hypnozoites within 5 days after invasion. This recruitment is also observed in P. vivax-infected reticulocytes. Chemical treatment with the AQP3 inhibitor auphen reduces P. vivax liver hypnozoite and schizont burden, and inhibits P. vivax asexual blood-stage growth. These findings reveal a role for AQP3 in P. vivax liver and blood stages and suggest that the protein may be targeted for therapeutic treatment.

间日疟原虫感染肝细胞以形成导致血液感染的裂殖体，或休眠的次生子，它们在肝脏中可持续存在数月，然后导致复发性血液感染。驱动P的分子过程。间日疟原虫裂殖体和hypnozoite生存仍是未知，但它们可能涉及丰富的宿主-病原体相互作用，包括那些在宿主-寄生虫界面发生的网络，寄生泡膜（PVM）。使用最近开发的P。间充质肝阶段模型系统，我们证明了宿主aquaporin-3（AQP3）在入侵后5天内定位于裂殖体和次生动物的PVM。在P中也观察到了这种招聘。间质感染的网状细胞。与AQP3抑制剂auphen化学治疗降低P。间日疟原虫肝hypnozoite和裂殖体的负担，抑制P。间质无性血液阶段生长。这些发现揭示了AQP3在P中的作用。间质肝和血液阶段，提示该蛋白可能是治疗目标。