Proteome of peripheral mononuclear cells (PBMCs) from asymptomatic malaria and uninfected individuals and the ensuing malaria episodes

Cumulative malaria parasite exposure in endemic regions often results in
the acquisition of partial immunity and asymptomatic infections. There is
limited information on how host-parasite interactions mediate maintenance
of chronic symptomless infections that sustain malaria transmission. Here,
we have determined the gene expression profiles of the parasite population
and the corresponding host peripheral blood mononuclear cells (PBMCs) from
21 children (<15 years). We compared children who were defined as
uninfected, asymptomatic and those with febrile malaria. Children with
asymptomatic infections had a parasite transcriptional profile
characterized by a bias toward trophozoite stage (~12 hours-post invasion)
parasites and low parasite levels, while earlier ring stage parasites were
characteristic of febrile malaria. The host response of asymptomatic
children was characterized by downregulated transcription of genes
associated with inflammatory responses, compared to children with febrile
malaria. Interestingly, the host responses during febrile infections that
followed an asymptomatic infection featured stronger inflammatory
responses, whereas the febrile host responses from previously uninfected
children featured increased humoral immune responses. The priming effect
of prior asymptomatic infection may explain the blunted acquisition of
antibody responses seen to malaria antigens following natural exposure or
vaccination in malaria endemic areas.