Preferential use of Siglec-1 or Siglec-10 by type 1 and type 2 PRRSV strains to infect PK15S1–CD163 and PK15S10–CD163 cells

• Main Authors: Jiexiong Xie, Isaura Christiaens, Bo Yang, Ivan Trus, Bert Devriendt, Tingting Cui, Ruifang Wei, Hans J. Nauwynck
• Format: Article
• Language: English
• Published: BMC 2018-07-01
• Series: Veterinary Research
• Online Access: http://link.springer.com/article/10.1186/s13567-018-0569-z

Abstract Cellular entry mediators define whether the cell is permissive to PRRSV infection. Porcine sialoadhesin (pSn, Siglec-1) and CD163 are main entry mediators facilitating infection of porcine macrophages by PRRSV. Recently, Siglec-10 was demonstrated to be an alternative receptor for PRRSV. To examine if virulence and pathogenicity of PRRSV strains could be correlated with the use of different Siglecs, a PK15 cell line recombinantly expressing Siglec-1 and CD163 (PK15S1–CD163) and a PK15 cell line recombinantly expressing Siglec-10 and CD163 (PK15S10–CD163) were used to compare the virus replication of 7 genotype 1 subtype 1 strains (G1s1), 2 genotype 1 subtype 3 (G1s3) strains and 5 genotype 2 (G2) strains. Some strains (08VA (G1s1), 13V117 (G1s1), 17V035 (G1s1), VR2332 (G2)) were poor virus producers (<104 TCID50/mL), while other strains (07V063 (G1s1), 13V091 (G1s1), Su1-Bel (G1s3), MN-184 (G2), Korea17 (G2) and SDSU-73 (G2)) easily grew up to ≥106 TCID50/mL. PK15S10–CD163 cells exhibited a higher efficiency in virus production per infected cell than the PK15S1–CD163 cells. The G1s1 strains LV and 07V063 infected more cells in the PK15S1–CD163, whereas the 94V360 and 08VA strains preferred PK15S10–CD163. The highly virulent G1s3 strains Lena and Su1-Bel showed a strong preference for PK15S1–CD163. The G2 strains MN-184, SDSU-73, Korea17 had a much higher infection rate in PK15S10–CD163, while the reference strain VR2332 and the NADC30 strain had a slight preference for PK15S1–CD163. Differences in receptor use may influence the outcome of a PRRSV infection in pigs and explain in part the virulence/pathogenicity of PRRSV strains.