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.
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Xie et al. (2018) studied this question.
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