RT Journal Article
SR Electronic
T1 Malaria abrogates O’nyong–nyong virus pathologies by restricting virus infection in nonimmune cells
JF Life Science Alliance
JO Life Sci. Alliance
FD Life Science Alliance LLC
SP e202101272
DO 10.26508/lsa.202101272
VO 5
IS 4
A1 Torres-Ruesta, Anthony
A1 Teo, Teck-Hui
A1 Chan, Yi-Hao
A1 Amrun, Siti Naqiah
A1 Yeo, Nicholas Kim-Wah
A1 Lee, Cheryl Yi-Pin
A1 Nguee, Samantha Yee-Teng
A1 Tay, Matthew Zirui
A1 Nosten, Francois
A1 Fong, Siew-Wai
A1 Lum, Fok-Moon
A1 Carissimo, Guillaume
A1 Renia, Laurent
A1 Ng, Lisa FP
YR 2022
UL http://www.life-science-alliance.org/content/5/4/e202101272.abstract
AB O’nyongnyong virus (ONNV) is a re-emerging alphavirus previously known to be transmitted by main malaria vectors, thus suggesting the possibility of coinfections with arboviruses in co-endemic areas. However, the pathological outcomes of such infections remain unknown. Using murine coinfection models, we demonstrated that a preexisting blood-stage Plasmodium infection suppresses ONNV-induced pathologies. We further showed that suppression of viremia and virus dissemination are dependent on Plasmodium-induced IFNγ and are associated with reduced infection of CD45− cells at the site of virus inoculation. We further proved that treatment with IFNγ or plasma samples from Plasmodium vivax–infected patients containing IFNγ are able to restrict ONNV infection in human fibroblast, synoviocyte, skeletal muscle, and endothelial cell lines. Mechanistically, the role of IFNγ in restricting ONNV infection was confirmed in in vitro infection assays through the generation of an IFNγ receptor 1 α chain (IFNγR1)–deficient cell line.