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Acquired clinical immunity to malaria in non-human primates co-infected with Schistosoma and Plasmodium parasites.

Ruth K NyakundiJann HauPaul OgongoOnkoba NyamongoMaamum JenebyMercy Y AkinyiIsaac MuleiFred NyundoIdle FarahIndu MalhotraHastings OzwaraChristopher L KingThomas Kariuki
Published in: Infection and immunity (2021)
Background. Naturally acquired immunity to malaria develops over several years and can be compromised by concomitant infections. This study explored the influence of chronic schistosomiasis on clinical outcome and immunity to repeated malaria infection. Methods. Two groups of baboons (n=8 each), were infected with Schistosoma mansoni cercariae to establish chronic infections. One of the two groups was treated with Praziquantel to eliminate schistosome infection. The two groups plus a new malaria control group (n=8), were inoculated three times with Plasmodium knowlesi parasites at one-month intervals. Clinical data, IgG, IgG1, memory T-cells and monocyte levels were recorded. Results. We observed after three P. knowlesi infections; i) reduced clinical symptoms in all groups with each subsequent infection, ii) increase IgG and IgG1in the malaria control (Pk-only) group iii) increased IgG and IgG1, CD14+ and CD14-CD16+ in the Schistosoma treated (Schisto/PZQ+Pk) group and iv) significantly lower IgG and IgG1 levels compared to Pk-only, reduced CD4+CD45RO+ and increased CD14-CD16+ cells in the co-infected (Schisto+Pk) group. Conclusion. Chronic S. mansoni does not compromise establishment of clinical immunity after multiple malaria infections with non-classical monocytes seeming to play a role. Failure to develop robust antibody and memory T-cells may have a long-term impact on acquired immunity to malaria infection.
Keyphrases
  • plasmodium falciparum
  • endothelial cells
  • dendritic cells
  • working memory
  • signaling pathway
  • cell proliferation
  • depressive symptoms
  • cell death
  • big data
  • endoplasmic reticulum stress