Plasmodium co-infection protects against chikungunya virus-induced pathologies

Teck-Hui Teo, Fok-Moon Lum, Khairunnisa Ghaffar, Yi-Hao Chan, Siti Naqiah Amrun, Jeslin J. L. Tan, Cheryl Y. P. Lee, Tze-Kwang Chua, Guillaume Carissimo, Wendy W. L. Lee, Carla Claser, Ravisankar Rajarethinam, Laurent Rénia () and Lisa F. P. Ng ()
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Teck-Hui Teo: Technology and Research (A*STAR)
Fok-Moon Lum: Technology and Research (A*STAR)
Khairunnisa Ghaffar: Technology and Research (A*STAR)
Yi-Hao Chan: Technology and Research (A*STAR)
Siti Naqiah Amrun: Technology and Research (A*STAR)
Jeslin J. L. Tan: Technology and Research (A*STAR)
Cheryl Y. P. Lee: Technology and Research (A*STAR)
Tze-Kwang Chua: Technology and Research (A*STAR)
Guillaume Carissimo: Technology and Research (A*STAR)
Wendy W. L. Lee: Technology and Research (A*STAR)
Carla Claser: Technology and Research (A*STAR)
Ravisankar Rajarethinam: Technology and Research (A*STAR)
Laurent Rénia: Technology and Research (A*STAR)
Lisa F. P. Ng: Technology and Research (A*STAR)

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Co-infection with Plasmodium and chikungunya virus (CHIKV) has been reported in humans, but the impact of co-infection on pathogenesis remains unclear. Here, we show that prior exposure to Plasmodium suppresses CHIKV-associated pathologies in mice. Mechanistically, Plasmodium infection induces IFNγ, which reduces viraemia of a subsequent CHIKV infection and suppresses tissue viral load and joint inflammation. Conversely, concomitant infection with both pathogens limits the peak of joint inflammation with no effect on CHIKV viraemia. Reduced peak joint inflammation is regulated by elevated apoptosis of CD4+ T-cells in the lymph nodes and disrupted CXCR3-mediated CD4+ T-cell migration that abolishes their infiltration into the joints. Virus clearance from tissues is delayed in both infection scenarios, and is associated with a disruption of B cell affinity-maturation in the spleen that reduces CHIKV-neutralizing antibody production.

Date: 2018
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DOI: 10.1038/s41467-018-06227-9

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