Porcine reproductive and respiratory syndrome virus (PRRSV) has been epidemic more than 30 years in America and 20 years in China. It is still one of the most important causative agents to the worldwide swine industry. Here, we systematically analyzed the prevalence status of PRRSV in China by a molecular epidemiological perspective. Now both PRRSV-1 and PRRSV-2 are circulating and approximately more than 80% of pig farms are seropositive for PRRSV. For PRRSV-2, there are four lineages (lineage 1, lineage 3, lineage 5, lineage 8) circulating in the fields. Lineage 8 (CH-1a-like) and lineage 5 (BJ-4-like) appeared almost at the same time during 1995-1996. Notably, BJ-4 shares 99.6% and 99.8% identity with VR2332 and RespPRRS MLV, respectively. It means that lineage 5 is likely to be imported from America. Now highly pathogenic PRRSV (HP-PRRSV) which was considered to be evolved from local diversity of lineage 8 strains is predominant with different variants. Lineage 3 appeared in 2010 which is mainly sporadic in south of China. Lineage 1, also known as NADC30-like strains in China, has been prevalent since 2013 and leads to PRRS pandemic again. For PRRSV-1, although sporadic at present, more than 9 provinces/regions have been reported. All the circulating strains belong to subtype I. It should be paid more attention since there are no vaccines available. Our analysis would help to deeply understand the prevalent status of PRRSV in China and provide useful information for prevention and control of porcine reproductive and respiratory syndrome (PRRS).

Porcine reproductive and respiratory syndrome (PRRS) has become an economically critical factor in swine industry since its worldwide spread in the 1990s. Infection by its causative agent, PRRS virus (PRRSV), was proven to be mediated by an indispensable receptor, porcine CD163 (pCD163), and the fifth scavenger receptor cysteine-rich domain (SRCR5) is essential for virus infection. However, the structural details and specific residues of pCD163 SRCR5 involved in infection have not been defined yet. In this study, we prepared recombinant pCD163 SRCR5 inDrosophila melanogasterSchneider 2 (S2) cells and determined its crystal structure at a high resolution of 2.0 Å. This structure includes a markedly long loop region and shows a special electrostatic potential, and these are significantly different from those of other members of the scavenger receptor cysteine-rich superfamily (SRCR-SF). Subsequently, we carried out structure-based mutational studies to identify that the arginine residue at position 561 (Arg561) in the long loop region is important for PRRSV infection. Further, we showed Arg561 probably takes effect on the binding of pCD163 to PRRSV during virus invasion. Altogether the current work provides the first view of the CD163 SRCR domain, expands our knowledge of the invasion mechanism of PRRSV, and supports a molecular basis for prevention and control of the virus.IMPORTANCEPRRS has caused huge economic losses to pig farming. The syndrome is caused by PRRSV, and PRRSV infection has been shown to be mediated by host cell surface receptors. One of them, pCD163, is especially indispensable, and its SRCR5 domain has been further demonstrated to play a significant role in virus infection. However, its structural details and the residues involved in infection are unknown. In this study, we determined the crystal structure of pCD163 SRCR5 and then carried out site-directed mutational studies based on the crystal structure to elucidate which residue is important. Our work not only provides structural information on the CD163 SRCR domain for the first time but also indicates the molecular mechanism of PRRSV infection and lays a foundation for future applications in prevention and control of PRRS.