Standard strategies for control of porcine reproductive and respiratory syndrome virus (PRRSV) have not been effective, as vaccines have not reduced the prevalence of disease and many producers depopulate after an outbreak. Another method of control would be to prevent the virus from infecting the pig. The virus was thought to infect alveolar macrophages by interaction with a variety of cell surface molecules. One popular model had PRRSV first interacting with heparin sulfate followed by binding to sialoadhesin and then being internalized into an endosome. Within the endosome, PRRSV was thought to interact with CD163 to uncoat the virus so the viral genome could be released into the cytosol and infect the cell. Other candidate receptors have included vimentin, CD151 and CD209. By using genetic engineering, it is possible to test the importance of individual entry mediators by knocking them out. Pigs engineered by knockout of sialoadhesin were still susceptible to infection, while CD163 knockout resulted in pigs that were resistant to infection. Genetic engineering is not only a valuable tool to determine the role of specific proteins in infection by PRRSV (in this case), but also provides a means to create animals resistant to disease. Genetic engineering of alveolar macrophages can also illuminate the role of other proteins in response to infection. We suggest that strategies to prevent infection be pursued to reduce the reservoir of virus.
Keywords: CD163; Genetic engineering; PRRSV; Receptor; Resistance.
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