PRRS virus receptors and their role for pathogenesis

• We review putative receptor molecules for PRRS virus.
• Six molecules have been reported so far as receptors for PRRS virus.
• CD163 and sialoadhesin are most extensively studied.
• CD163 expression confers PRRSV-non-permissive cells to permissive.
• Sialoadhesin-knockout transgenic pigs remain to be susceptible for PRRS virus infection.

Porcine reproductive and respiratory syndrome virus (PRRSV) is endemic in most pig producing countries worldwide and causes enormous economic losses to the swine industry. Specifically differentiated porcine alveolar macrophages are the primary target for PRRSV infection in pigs. At least six cellular molecules have been described so far as putative receptors for PRRSV, and they include heparan sulfate, vimentin, CD151, sialoadhesin (CD169; siglec-1), dendritic cell-specific intercellular adhesion melecule-3-grabbing non-integrin (DC-SIGN; CD209), and CD163 (SRCR, cysteine-rich scavenger receptor). Progress has been made to shed light on the interactions between cells and PRRSV, and this review describes the advances and current understanding of the entry of PRRSV to cells with a particular focus on the role of CD163 and sialoadhesin for infection and PRRSV pathogenesis. CD163 is most likely the primary and core receptor for PRRSV and determines the susceptibility of cells to the virus. Sialoadhesin is either unnecessary for infection or may function as an accessory protein. Sialoadhesin has been mostly studied for genotype I PRRSV whereas the utilization of CD163 has been mostly studied using genotype II PRRSV, and whether each genotype indeed utilizes a different receptor is unclear.