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. 2020 Jan 13;10:3115. doi: 10.3389/fmicb.2019.03115

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Copyright © 2020 Yu, Wei, Dong, Zhu, Zhang, Chen, Liu and Guo.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic model of PRRSV life cycle in CD163^WT and CD163^ΔSRCR5 cells. In CD163^WT cells, after virions internalize into early endosomes, viral glycoproteins (GP2a, 3, 4, and 5) interact with the CD163 receptor and host proteins such as calpain 1, thus facilitating virus uncoating from early endosomes to release genome to the cytoplasm. Subsequently, the viral genome initiates its replication. However, after virions traffic to early endosomes and meet with CD163^ΔSRCR5 in CD163^ΔSRCR5 cells, only viral GP4 interacts with the CD163^ΔSRCR5 receptor and calpain 1 fails to interact with SRCR5 domain. Due to the failed interaction among CD163^ΔSRCR5, viral glycoproteins and calpain 1, virus uncoating is blocked in the early endosomes and virions are forced to the late endosomes and finally to the lysosomes, where they are degraded.