Preferential use of Siglec-1 or Siglec-10 by type 1 and type 2 PRRSV strains to infect PK15(S1–CD163) and PK15(S10–CD163) cells

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 (PK15(S1–CD163)) and a PK15 cell line recombinantly expressing Siglec-10 and CD163 (PK15(S10–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 (<10(4) TCID(50)/mL), while other strains (07V063 (G1s1), 13V091 (G1s1), Su1-Bel (G1s3), MN-184 (G2), Korea17 (G2) and SDSU-73 (G2)) easily grew up to ≥10(6) TCID(50)/mL. PK15(S10–CD163) cells exhibited a higher efficiency in virus production per infected cell than the PK15(S1–CD163) cells. The G1s1 strains LV and 07V063 infected more cells in the PK15(S1–CD163), whereas the 94V360 and 08VA strains preferred PK15(S10–CD163). The highly virulent G1s3 strains Lena and Su1-Bel showed a strong preference for PK15(S1–CD163). The G2 strains MN-184, SDSU-73, Korea17 had a much higher infection rate in PK15(S10–CD163), while the reference strain VR2332 and the NADC30 strain had a slight preference for PK15(S1–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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13567-018-0569-z) contains supplementary material, which is available to authorized users.