Genome-Wide Scans for Ghanaian Plasmodium falciparum Genes Under Selection From Local and Chinese Host Populations.

Shan-Mei Shi,Yan-Bing Cui,Jun-Hu Chen,Moses Okpeku,Hai-Mo Shen,Shen-Bo Chen,Kokouvi Kassegne,Tian-Qi Shi

doi:10.3389/fcimb.2021.630797

Abstract

Initial malarial infection mostly causes symptomatic illness in humans. Infection that is not fatal induces complete protection from severe illness and death, and thus complete protection from severe illness or death is granted with sufficient exposure. However, malaria parasite immunity necessitates constant exposure. Therefore, it is important to evaluate lowered immunity and recurrent susceptibility to symptomatic disease in lower transmission areas. We aimed to investigate selection pressure based on transmission levels, antimalarial drug use, and environmental factors. We whole genome sequenced (WGS) P. falciparum clinical samples from Chinese hosts working in Ghana and compared the results with the WGS data of isolates from native Ghanaians downloaded from pf3k. The P. falciparum samples were generally clustered according to their geographic origin, and Chinese imported samples showed a clear African origin with a slightly different distribution from the native Ghanaian samples. Moreover, samples collected from two host populations showed evidence of differences in the intensity of selection. Compared with native Ghanaian samples, the China-imported isolates exhibited a higher proportion of monoclonal infections, and many genes associated with RBC invasion and immune evasion were found to be under less selection pressure. There was no significant difference in the selection of drug-resistance genes due to a similar artemisinin-based combination therapy medication profile. Local selection of malarial parasites is considered to be a result of differences in the host immunity or disparity in the transmission opportunities of the host. In China, most P. falciparum infections were imported from Africa, and under these circumstances, distinct local selective pressures may be caused by varying acquired immunity and transmission intensity. This study revealed the impact of host switching on the immune system, and it may provide a better understanding of the mechanisms that enable clinical immunity to malaria.

Highlights

Malarial parasites have yielded to the selection pressure of host immune systems after coexisting and interacting with their hosts for over 150 million years. (Carter and Mendis, 2002)
Our results deepen our understanding of factors that might drive clinical immunity against malaria
We hypothesized that the imported population should exhibit a higher proportion of monoclonal infections, and many genes/ gene families associated with red blood cells (RBCs) invasion and immune evasion are under less selection pressures

Summary

Introduction

Malarial parasites have yielded to the selection pressure of host immune systems after coexisting and interacting with their hosts for over 150 million years. (Carter and Mendis, 2002). (Ryg-Cornejo et al, 2016) In this process, infants may develop lethal febrile illness, but adults acquire complete protection from severe illness or death, even though some believe that sterile immunity can never be achieved (Simon et al, 2015). Research has focused on lowered immunity and recurrent susceptibility to symptomatic disease in lower transmission areas (Barry and Hansen, 2016). During this long-term fight between humans and malaria, almost all surface antigens of the parasite have been tested for vaccine development, and their extensive polymorphisms from geographical distribution are considered to slow down the development of acquired immunity (Doolan et al, 2009; Barry and Arnott, 2014)

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