CD163 and viral infectious disease: Further, deleted and chimeric mutants of CD163 were performed to confirm that scavenger receptor cysteine-rich domain 5–9 (SRCR5–9) domain was an interaction site for the virus, which was critical for virus infection [30], while the other four SRCRs at the N-terminal and the cytoplasmic tail were not required for CD163 to sustain PRRSV infection [24].