Phenotypic and fitness consequences of plasticity in the rhythmic replication of malaria parasites.

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The environments that parasites experience within hosts change dramatically over 24 h. How rhythms shape host-parasite-vector interactions is poorly understood owing to the challenges of disentangling the roles of rhythms of multiple interacting species in the context of the complex lifecycles of parasites. Using canonical circadian clock-disrupted hosts, we probe the limits of flexibility in the rhythmic replication of malaria (Plasmodium) parasites and quantify the consequences for fitness proxies of both parasite and host. We reveal that parasites alter the duration of their replication rhythm to resonate with host rhythms that have short (21 h) daily T-cycles as accurately as when infecting hosts with 24 h cycles, but appear less capable of extending their replication rhythm in hosts with long (27 h) cycles. Despite matching the period of short T-cycle hosts, parasites are unable to lock to the correct phase, likely leading to lower within-host productivity and a reduction in transmission potential. However, parasites in long T-cycle hosts do not experience substantial fitness costs. Furthermore, T-cycle duration does not affect disease severity in clock-disrupted hosts. Understanding the rhythmic replication of malaria parasites offers the opportunity to interfere with parasite timing to improve health and reduce transmission.This article is part of the Theo Murphy meeting issue issue 'Circadian rhythms in infection and immunity'.