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Title: Malaria abrogates O'nyong-nyong virus pathologies by restricting virus infection in nonimmune cells
Authors: Torres-Ruesta, Anthony
Teo, Teck-Hui
Chan, Yi-Hao
Siti Naqiah Amrun
Yeo, Nicholas Kim-Wah
Lee, Cheryl Yi-Pin
Nguee, Samantha Yee-Teng
Tay, Matthew Zirui
Nosten, Francois
Fong, Siew-Wai
Lum, Fok-Moon
Carissimo, Guillaume
Renia, Laurent
Ng, Lisa F. P.
Keywords: Science::Medicine
Issue Date: 2022
Source: Torres-Ruesta, A., Teo, T., Chan, Y., Siti Naqiah Amrun, Yeo, N. K., Lee, C. Y., Nguee, S. Y., Tay, M. Z., Nosten, F., Fong, S., Lum, F., Carissimo, G., Renia, L. & Ng, L. F. P. (2022). Malaria abrogates O'nyong-nyong virus pathologies by restricting virus infection in nonimmune cells. Life Science Alliance, 5(4), e202101272-.
Project: NRF2017_SISFP09
Journal: Life Science Alliance
Abstract: 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.
ISSN: 2575-1077
DOI: 10.26508/lsa.202101272
Rights: © 2022 Torres-Ruesta et al. This article is available under a Creative Commons License (Attribution 4.0 International, as described at
Fulltext Permission: open
Fulltext Availability: With Fulltext
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