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Contrasting genomic epidemiology between sympatric Plasmodium falciparum and Plasmodium vivax populations

Schwabl, P.; Camponovo, F.; Clementson, C.; Early, A. M.; Laws, M.; Forero-Pena, D. A.; Noya, O.; Grillet, M. E.; Vanhove, M.; Anthony, F.; James, K.; Singh, N.; Cox, H.; Niles-Robin, R.; Buckee, C. O.; Neafsey, D. E.

2024-04-22 infectious diseases
10.1101/2024.04.22.24306174 medRxiv
Show abstract

The malaria parasites Plasmodium falciparum and Plasmodium vivax differ in key biological processes and associated clinical effects, but consequences on population-level transmission dynamics are difficult to predict. This co-endemic malaria study from Guyana details important epidemiological contrasts between the species by coupling population genomics (1,396 spatiotemporally-matched parasite genomes) with sociodemographic analysis (nationwide patient census). We describe how P. falciparum forms large, interrelated subpopulations that sporadically expand but generally exhibit restrained dispersal, whereby spatial distance and patient travel statistics predict parasite identity-by-descent (IBD). Case bias towards working-age adults is also strongly pronounced. P. vivax exhibits 46% higher average diversity ({pi}) and 6.5x lower average IBD. It occupies a wider geographic range, without evidence for outbreak-like expansions, only microgeographic patterns of isolation-by-distance, and weaker case bias towards adults. Possible latency-relapse effects also manifest in various analyses. For example, 11.0% of patients diagnosed with P. vivax in Greater Georgetown report no recent travel to endemic zones, and P. vivax clones recur in 11/46 patients incidentally sampled twice during the study. Polyclonality rate is also 2.1x higher than in P. falciparum, does not trend positively with estimated incidence, and correlates uniquely to selected demographics. We discuss possible underlying mechanisms and implications for malaria control.

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