2. Academic Validation
  3. Acute Plasmodium Infection Promotes Interferon-Gamma-Dependent Resistance to Ebola Virus Infection

Acute Plasmodium Infection Promotes Interferon-Gamma-Dependent Resistance to Ebola Virus Infection

  • Cell Rep. 2020 Mar 24;30(12):4041-4051.e4. doi: 10.1016/j.celrep.2020.02.104.
Kai J Rogers 1,  Olena Shtanko 2,  Rahul Vijay 1,  Laura N Mallinger 1,  Chester J Joyner 3,  Mary R Galinski 4,  Noah S Butler 5,  Wendy Maury 6
Affiliations

Affiliations

  • 1 Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242, USA.
  • 2 Host-Pathogen Interactions, Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
  • 3 Division of Pulmonary, Allergy, Critical Care & Sleep Medicine, Department of Medicine, Emory University, Atlanta, GA 30322, USA; Malaria Host-Pathogen Interaction Center, Emory Vaccine Center, Yerkes National Primate Center, Emory University, Atlanta, GA 30322, USA.
  • 4 Malaria Host-Pathogen Interaction Center, Emory Vaccine Center, Yerkes National Primate Center, Emory University, Atlanta, GA 30322, USA; Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
  • 5 Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242, USA; Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242, USA.
  • 6 Department of Microbiology and Immunology, University of Iowa, Iowa City, IA 52242, USA; Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242, USA. Electronic address: wendy-maury@uiowa.edu.
PMID: 32209467 DOI: 10.1016/j.celrep.2020.02.104
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.

Keywords

Ebola virus; Plasmodium; co-infection; filovirus; innate immunity; interferon gamma; macrophage; macrophage polarization; malaria.

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