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

The environment that parasites experience within their host changes dramatically over 24 hours. How rhythms shape host-parasite-vector interactions is poorly understood due 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 hour) daily T-cycles as accurately as when infecting host with 24 hour cycles, but are unable to extend their replication rhythm in hosts with long (27 hour) cycles. Despite matching the period of short T-cycle hosts, parasites are unable to lock to the correct phase, resulting in 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.