Abstract
Cellular receptors play a critical role in viral infection. At least seven cellular molecules have been identified as putative viral entry mediators for porcine reproductive and respiratory syndrome virus (PRRSV). Accumulating data indicate that among these candidates, CD163, a cysteine-rich scavenger receptor on macrophages, is the major receptor for PRRSV. This review discusses the recent advances and understanding of the entry of PRRSV into cells, viral pathogenesis in CD163 gene-edited swine, and CD163 as a potential target of receptor–ligand for the control of PRRS.
Highlights
Infections caused by porcine reproductive and respiratory syndrome virus (PRRSV)
For PRRSV, Suidae sus is the only natural host, and in vitro, viral infection is limited to differentiated blood monocytes (BMo) and a subset of primary porcine alveolar macrophages (PAMs) [28,29]
These results suggest that different genotypes and strains of PRRSV may preferentially utilize different siglec molecules
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Infections caused by porcine reproductive and respiratory syndrome virus (PRRSV). Two genotypes have been described for PRRSV: PRRSV-1 (European genotype; Betaarterivirus suid 1) and PRRSV-2 (North American genotype; Betaarterivirus suid 2) Both types cause a similar clinical disease but share only approximately 60% nucleotide sequence identity at the genome level [1,3,4,5,6]. SHFV infects monkeys and in vitro; it is limited to simian primary macrophages and African green monkey kidney-derived cell lines, such as MA-104 [22]. For PRRSV, Suidae sus is the only natural host, and in vitro, viral infection is limited to differentiated blood monocytes (BMo) and a subset of primary porcine alveolar macrophages (PAMs) [28,29]. MA-104 and MARC-145 are susceptible to PRRSV and are commonly used for virus research in vitro and virus propagation for vaccines [30,31]
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