| Literature DB >> 32209467 |
Kai J Rogers1, Olena Shtanko2, Rahul Vijay1, Laura N Mallinger1, Chester J Joyner3, Mary R Galinski4, Noah S Butler5, Wendy Maury6.
Abstract
During the 2013-2016 Ebola virus (EBOV) epidemic, a significant number of patients admitted to Ebola treatment units were co-infected with Plasmodium falciparum, a predominant agent of malaria. However, there is no consensus on how malaria impacts EBOV infection. The effect of acute Plasmodium infection on EBOV challenge was investigated using mouse-adapted EBOV and a biosafety level 2 (BSL-2) model virus. We demonstrate that acute Plasmodium infection protects from lethal viral challenge, dependent upon interferon gamma (IFN-γ) elicited as a result of parasite infection. Plasmodium-infected mice lacking the IFN-γ receptor are not protected. Ex vivo incubation of naive human or mouse macrophages with sera from acutely parasitemic rodents or macaques programs a proinflammatory phenotype dependent on IFN-γ and renders cells resistant to EBOV infection. We conclude that acute Plasmodium infection can safeguard against EBOV by the production of protective IFN-γ. These findings have implications for anti-malaria therapies administered during episodic EBOV outbreaks in Africa.Entities:
Keywords: Ebola virus; Plasmodium; co-infection; filovirus; innate immunity; interferon gamma; macrophage; macrophage polarization; malaria
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Year: 2020 PMID： 32209467 PMCID： PMC7172281 DOI： 10.1016/j.celrep.2020.02.104
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423