Open AccessA Virus Hosted in Malaria-Infected Blood Protects against T Cell-Mediated Inflammatory Diseases by Impairing DC Function in a Type I IFN-Dependent Manner
Author(s) -
Ali Hassan,
Myriam F. Wlodarczyk,
Mehdi Benamar,
Emilie Bassot,
Anna Salvioni,
Sahar Kassem,
Antoine Berry,
Abdelhadi Saoudi,
Nicolas Blanchard
Publication year - 2020
Publication title -
mbio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.562
H-Index - 121
eISSN - 2161-2129
pISSN - 2150-7511
DOI - 10.1128/mbio.03394-19
Subject(s) - plasmodium berghei , cerebral malaria , malaria , plasmodium yoelii , immunology , immune system , biology , virus , virology , plasmodium (life cycle) , interferon , plasmodium falciparum , parasite hosting , parasitemia , world wide web , computer science
Any infection modifies the host immune status, potentially ameliorating or aggravating the pathophysiology of a simultaneous inflammatory condition. In the course of investigating how malaria infection modulates the severity of contemporaneous inflammatory diseases, we identified a nonpathogenic mouse virus in stabilates of two widely used rodent parasite lines: Plasmodium berghei K173 and Plasmodium yoelii 17X YM. We established that the protective effects of these Plasmodium lines on cerebral malaria and multiple sclerosis are exclusively due to this virus. The virus induces a massive type I interferon (IFN-I) response and causes quantitative and qualitative defects in the ability of dendritic cells to promote pathogenic T cell responses. Beyond revealing a possible confounding factor in rodent malaria models, our work uncovers some bases by which a seemingly innocuous viral (co)infection profoundly changes the immunopathophysiology of inflammatory diseases.