Acute Plasmodium Infection Promotes Interferon-Gamma-Dependent Resistance to Ebola Virus Infection.
Cell Rep
; 30(12): 4041-4051.e4, 2020 03 24.
Article
in En
| MEDLINE
| ID: mdl-32209467
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.
Key words
Full text:
1
Collection:
01-internacional
Health context:
1_ASSA2030
/
2_ODS3
/
3_ND
Database:
MEDLINE
Main subject:
Plasmodium falciparum
/
Interferon-gamma
/
Hemorrhagic Fever, Ebola
/
Ebolavirus
/
Disease Resistance
/
Malaria
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Cell Rep
Year:
2020
Document type:
Article