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An intact sialoadhesin (Sn/SIGLEC1/CD169) is not required for attachment/internalization of the porcine reproductive and respiratory syndrome virus (PRRSV)

The results demonstrate that the expression of the SIGLEC1 gene is not required for infection of pigs with PRRSV and the absence of SIGLEC1 does not contribute to the pathogenesis of acute disease.

7 August 2013
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Surface expression of SIGLEC1, also known as sialoadhesin (SN) or CD169, is considered a primary determinant for the permissiveness of porcine alveolar macrophages (PAMs) for infection by porcine reproductive and respiratory syndrome virus (PRRSV). In vitro the attachment and internalization of PRRSV is dependent on the interaction between sialic acid on the virion surface and the sialic acid binding domain of the SIGLEC1 gene.

To test the role of SIGLEC1 in PRRSV infection, a SIGLEC1 gene knockout pig was created by removing part of exon 1 and all of exons 2 and 3 of the SIGLEC1 gene. The resulting knockout ablated SIGLEC1 expression on the surface of alveolar macrophages, but had no effect on the expression of CD163, a co-receptor for PRRSV. After infection, PRRSV viremia in SIGLEC1 −/− pigs followed the same course as −/+ and +/+ litter mates. The absence of SIGLEC1 had no measurable effect on other aspects of PRRSV infection, including clinical disease course and histopathology.

The results demonstrate that the expression of the SIGLEC1 gene is not required for infection of pigs with PRRSV and the absence of SIGLEC1 does not contribute to the pathogenesis of acute disease.

Randall S. Prather, et al. An intact sialoadhesin (Sn/SIGLEC1/CD169) is not required for attachment/internalization of the porcine reproductive and respiratory syndrome virus (PRRSV). Journal of Virology. Published ahead of print 19 June 2013, doi: 10.1128/JVI.00177-13 JVI.00177-13

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