Cryptosporidium uses CSpV1 to activate host type I interferon and attenuate antiparasitic defenses

Silu Deng, Wei He, Ai-Yu Gong, Min Li, Yang Wang, Zijie Xia, Xin-Tiang Zhang, Andrew S. Huang Pacheco, Ankur Naqib, Mark Jenkins, Patrick C. Swanson, Kristen M. Drescher, Juliane K. Strauss-Soukup, Michael Belshan and Xian-Ming Chen ()
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Silu Deng: Rush University Medical Center
Wei He: Creighton University School of Medicine
Ai-Yu Gong: Rush University Medical Center
Min Li: Creighton University School of Medicine
Yang Wang: Creighton University School of Medicine
Zijie Xia: Creighton University School of Medicine
Xin-Tiang Zhang: Creighton University School of Medicine
Andrew S. Huang Pacheco: University of Nebraska Medical Center
Ankur Naqib: Rush University Medical Center
Mark Jenkins: the United States Department of Agriculture
Patrick C. Swanson: Creighton University School of Medicine
Kristen M. Drescher: Creighton University School of Medicine
Juliane K. Strauss-Soukup: Creighton University College of Arts and Sciences
Michael Belshan: Creighton University School of Medicine
Xian-Ming Chen: Rush University Medical Center

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract Cryptosporidium infects gastrointestinal epithelium and is a leading cause of infectious diarrhea and diarrheal-related death in children worldwide. There are no vaccines and no fully effective therapy available for the infection. Type II and III interferon (IFN) responses are important determinants of susceptibility to infection but the role for type I IFN response remains obscure. Cryptosporidium parvum virus 1 (CSpV1) is a double-stranded RNA (dsRNA) virus harbored by Cryptosporidium spp. Here we show that intestinal epithelial conditional Ifnar1−/− mice (deficient in type I IFN receptor) are resistant to C. parvum infection. CSpV1-dsRNAs are delivered into host cells and trigger type I IFN response in infected cells. Whereas C. parvum infection attenuates epithelial response to IFN-γ, loss of type I IFN signaling or inhibition of CSpV1-dsRNA delivery can restore IFN-γ-mediated protective response. Our findings demonstrate that type I IFN signaling in intestinal epithelial cells is detrimental to intestinal anti-C. parvum defense and Cryptosporidium uses CSpV1 to activate type I IFN signaling to evade epithelial antiparasitic response.

Date: 2023
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DOI: 10.1038/s41467-023-37129-0

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