Zhang Xiaoxiao, Guo Chunhe
Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, College of Veterinary Medicine, South China Agricultural University, Guangzhou, Guangdong, China.
Guangdong Laboratory for Lingnan Modern Agriculture, Guangzhou, Guangdong, China.
Front Microbiol. 2022 Sep 16;13:1006464. doi: 10.3389/fmicb.2022.1006464. eCollection 2022.
Porcine reproductive and respiratory syndrome virus (PRRSV) has plagued the pig industry for more than 30 years and causes great economic losses. At present different commercial vaccines are available but limited tools. Until now at least six potential host factors are identified as the key receptors for PRRSV infection. Among them, CD163 molecule is the most important and critical in PRRSV life cycle responsible for mediating virus uncoating and genome release. It determines the susceptibility of target cells to the virus. Several PRRSV non-permissive cells (such as PK-15, 3D4/21, and BHK-21) are demonstrated to become completely susceptible to PRRSV infection in the presence of expression of porcine CD163 protein. Therefore, CD163 has become the target for the design of novel antiviral molecules disrupting the interaction between CD163 and viral glycoproteins, or the breeding of gene-modified animals against PRRSV infection. In this review, we comprehensively summarize the recent progress in inhibition of PRRSV replication targeting CD163 receptor. In addition, whether there are other potential molecules interacting with CD163 in the process of uncoating of virus life cycle is also discussed.
猪繁殖与呼吸综合征病毒（PRRSV）困扰养猪业30多年，造成巨大经济损失。目前虽有不同的商业疫苗，但手段有限。截至目前，至少已鉴定出六种潜在的宿主因子作为PRRSV感染的关键受体。其中，CD163分子在PRRSV生命周期中最为重要且关键，负责介导病毒脱壳和基因组释放。它决定了靶细胞对该病毒的易感性。一些PRRSV非允许细胞（如PK - 15、3D4/21和BHK - 21）在表达猪CD163蛋白时，被证明对PRRSV感染完全易感。因此，CD163已成为设计破坏CD163与病毒糖蛋白之间相互作用的新型抗病毒分子，或培育抗PRRSV感染的基因编辑动物的靶点。在本综述中，我们全面总结了针对CD163受体抑制PRRSV复制的最新进展。此外，还讨论了在病毒生命周期脱壳过程中是否存在其他与CD163相互作用的潜在分子。
