Redistribution of Endosomal Membranes to the African Swine Fever Virus Replication Site
Miguel Ángel Cuesta-Geijo,
Lucía Barrado-Gil,
Inmaculada Galindo,
Raquel Muñoz-Moreno,
Covadonga Alonso
Affiliations
Miguel Ángel Cuesta-Geijo
Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, INIA, Ctra. de la Coruña Km 7.5, 28040 Madrid, Spain
Lucía Barrado-Gil
Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, INIA, Ctra. de la Coruña Km 7.5, 28040 Madrid, Spain
Inmaculada Galindo
Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, INIA, Ctra. de la Coruña Km 7.5, 28040 Madrid, Spain
Raquel Muñoz-Moreno
Department of Microbiology and Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
Covadonga Alonso
Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, INIA, Ctra. de la Coruña Km 7.5, 28040 Madrid, Spain
African swine fever virus (ASFV) infection causes endosomal reorganization. Here, we show that the virus causes endosomal congregation close to the nucleus as the infection progresses, which is necessary to build a compact viral replication organelle. ASFV enters the cell by the endosomal pathway and reaches multivesicular late endosomes. Upon uncoating and fusion, the virus should exit to the cytosol to start replication. ASFV remodels endosomal traffic and redistributes endosomal membranes to the viral replication site. Virus replication also depends on endosomal membrane phosphoinositides (PtdIns) synthesized by PIKfyve. Endosomes could act as platforms providing membranes and PtdIns, necessary for ASFV replication. Our study has revealed that ASFV reorganizes endosome dynamics, in order to ensure a productive infection.
