| First Author | Rogers KJ | Year | 2020 |
| Journal | Cell Rep | Volume | 30 |
| Issue | 12 | Pages | 4041-4051.e4 |
| PubMed ID | 32209467 | Mgi Jnum | J:337102 |
| Mgi Id | MGI:6416685 | Doi | 10.1016/j.celrep.2020.02.104 |
| Citation | Rogers KJ, et al. (2020) Acute Plasmodium Infection Promotes Interferon-Gamma-Dependent Resistance to Ebola Virus Infection. Cell Rep 30(12):4041-4051.e4 |
| abstractText | 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-gamma) elicited as a result of parasite infection. Plasmodium-infected mice lacking the IFN-gamma 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-gamma and renders cells resistant to EBOV infection. We conclude that acute Plasmodium infection can safeguard against EBOV by the production of protective IFN-gamma. These findings have implications for anti-malaria therapies administered during episodic EBOV outbreaks in Africa. |
