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Porcine reproductive and respiratory syndrome (PRRS) was first described as a new disease in pig herds in North America late in the 1980s and beginning of the 1990s in Europe and is characterized by respiratory disease in young piglets and late-term reproductive failure. The causative agent of the disease was identified in Europe in 1991 and in the US in 1992 as a virus, PRRS virus (PRRSV). PRRSV is classified with equine arteritis virus (EAV), lactate dehydrogenaseelevating virus (LDV), and simian hemorrhagic fever virus (SHFV) in the family Arteriviridae, which is grouped with the Coronaviridae and the Roniviridae in the order Nidovirales. The virus is an enveloped particle with a diameter of 50 to 65 nm and contains a polyadenylated, positive-strand RNA genome. The genome is about 15 kDa and encodes 9 open reading frames: ORF1a and 1b code for nonstructural proteins, ORF2a, 2b, 3, 4, 5 and 6 code for structural membrane proteins, and ORF7 codes for the nucleocapsid protein (N). Currently, PRRSV is present in most, if not all swine-producing areas of the world, including North and South America, Western and Eastern Europe, and Asia. As the virus is now enzootic in most countries, the number of acute disease outbreaks has diminished and infections are in general mild and subclinical. From an economical point of view, however, the virus still causes major losses and is considered as the most important pig disease worldwide. Characteristic for all members of the Arteriviridae is not only that they have a very narrow host tropism, but also that they share a marked in vivo tropism for cells of the monocyte/macrophage lineage. 15

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Porcine Arterivirus Entry in Macrophages: Heparan Sulfate – Mediated Attachment, Sialoadhesin-Mediated Internalization, and a Cell-Specific Factor Mediating Virus Disassembly and Genome Release