Identification of CCZ1 as an essential lysosomal trafficking regulator in Marburg and Ebola virus infections

Vanessa Monteil(Karolinska University Hospital), Hyesoo Kwon(Swedish Veterinary Agency), Lijo John(Swedish Veterinary Agency), Cristiano Salata(University of Padua), Gustav Jonsson(Institute of Molecular Biotechnology), Sabine U. Vorrink(Karolinska Institutet), Sofia Appelberg(Public Health Agency of Sweden), Sonia Youhanna(Karolinska Institutet), Matheus Dyczynski, Alexandra Leopoldi(Institute of Molecular Biotechnology), Nicole Leeb(Institute of Molecular Biotechnology), Jennifer Volz(Institute of Molecular Biotechnology), Astrid Hagelkrüys(Institute of Molecular Biotechnology), Max J. Kellner(Institute of Molecular Biotechnology), Stéphanie Devignot(Karolinska University Hospital), Georg Michlits, Michelle Foong-Sobis(Institute of Molecular Biotechnology), Friedemann Weber(Justus-Liebig-Universität Gießen), Volker M. Lauschke(Karolinska Institutet), Moritz Horn, Heinz Feldmann(National Institutes of Health), Ulrich Elling(Institute of Molecular Biotechnology), Josef Penninger(Institute of Molecular Biotechnology), Alì Mirazimi(Public Health Agency of Sweden)
Nature Communications
October 25, 2023
Cited by 16Open Access
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Abstract

Marburg and Ebola filoviruses are two of the deadliest infectious agents and several outbreaks have occurred in the last decades. Although several receptors and co-receptors have been reported for Ebola virus, key host factors remain to be elucidated. In this study, using a haploid cell screening platform, we identify the guanine nucleotide exchange factor CCZ1 as a key host factor in the early stage of filovirus replication. The critical role of CCZ1 for filovirus infections is validated in 3D primary human hepatocyte cultures and human blood-vessel organoids, both critical target sites for Ebola and Marburg virus tropism. Mechanistically, CCZ1 controls early to late endosomal trafficking of these viruses. In addition, we report that CCZ1 has a role in the endosomal trafficking of endocytosis-dependent SARS-CoV-2 infections, but not in infections by Lassa virus, which enters endo-lysosomal trafficking at the late endosome stage. Thus, we have identified an essential host pathway for filovirus infections in cell lines and engineered human target tissues. Inhibition of CCZ1 nearly completely abolishes Marburg and Ebola infections. Thus, targeting CCZ1 could potentially serve as a promising drug target for controlling infections caused by various viruses, such as SARS-CoV-2, Marburg, and Ebola.


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