Cuesta-Geijo Miguel Ángel, Barrado-Gil Lucía, Galindo Inmaculada, Muñoz-Moreno Raquel, Alonso Covadonga
Department of Biotechnology, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, INIA, Ctra. de la Coruña Km 7.5, 28040 Madrid, Spain.
Department of Infectious Diseases, King's College London School of Medicine, Guy's Hospital, London SE1 9RT, UK.
Viruses. 2017 Jun 1;9(6):133. doi: 10.3390/v9060133.
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.
非洲猪瘟病毒(ASFV)感染会导致内体重新组织。在此,我们表明随着感染的进展,该病毒会使内体聚集在细胞核附近,这对于构建一个紧密的病毒复制细胞器是必要的。ASFV通过内体途径进入细胞并到达多囊泡晚期内体。在脱壳和融合后,病毒应释放到细胞质中以开始复制。ASFV重塑内体运输并将内体膜重新分布到病毒复制位点。病毒复制还依赖于由PIKfyve合成的内体膜磷酸肌醇(PtdIns)。内体可以作为提供ASFV复制所需的膜和PtdIns的平台。我们的研究表明,ASFV会重组内体动态,以确保产生有效的感染。