title: An intact sialoadhesin (Sn/SIGLEC1/CD169) is not required for attachment/internalization of the porcine reproductive and respiratory syndrome virus.
abstract: Surface expression of SIGLEC1, also known as sialoadhesin or CD169, is considered a primary determinant of the permissiveness of porcine alveolar macrophages for infection by porcine reproductive and respiratory syndrome virus (PRRSV). In vitro, the attachment and internalization of PRRSV are 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 coreceptor for PRRSV. After infection, PRRSV viremia in SIGLEC1(-/-) pigs followed the same course as in SIGLEC1(-/+) and SIGLEC1(+/+) littermates. 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 that the absence of SIGLEC1 does not contribute to the pathogenesis of acute disease.
authors.affiliation: Division of Animal Science, College of Food Agriculture and Natural Resources, University of Missouri, Columbia, Missouri, USA. pratherr@missouri.edu
authors.forename: Randall S
authors.initials: RS
authors.lastname: Prather
authors.forename: Raymond R R
authors.initials: RR
authors.lastname: Rowland
authors.forename: Catherine
authors.initials: C
authors.lastname: Ewen
authors.forename: Benjamin
authors.initials: B
authors.lastname: Trible
authors.forename: Maureen
authors.initials: M
authors.lastname: Kerrigan
authors.forename: Bhupinder
authors.initials: B
authors.lastname: Bawa
authors.forename: Jennifer M
authors.initials: JM
authors.lastname: Teson
authors.forename: Jiude
authors.initials: J
authors.lastname: Mao
authors.forename: Kiho
authors.initials: K
authors.lastname: Lee
authors.forename: Melissa S
authors.initials: MS
authors.lastname: Samuel
authors.forename: Kristin M
authors.initials: KM
authors.lastname: Whitworth
authors.forename: Clifton N
authors.initials: CN
authors.lastname: Murphy
authors.forename: Tina
authors.initials: T
authors.lastname: Egen
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Green
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D015703:Antigens, CD / Q000502:physiology; D015214:Antigens, Differentiation, Myelomonocytic / Q000502:physiology; D055786:Gene Knockout Techniques; D054884:Host-Pathogen Interactions / Q000276:immunology / Q000502:physiology; D016676:Macrophages, Alveolar / Q000276:immunology / Q000821:virology; D019318:Porcine Reproductive and Respiratory Syndrome / Q000276:immunology / Q000821:virology; D019316:Porcine respiratory and reproductive syndrome virus / Q000472:pathogenicity / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000502:physiology; D063267:Sialic Acid Binding Ig-like Lectin 1 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D034421:Sus scrofa; D013552:Swine; D053585:Virus Attachment; D053586:Virus Internalization; D000098902:CD163 Antigen
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D011956:Receptors, Cell Surface; D063267:Sialic Acid Binding Ig-like Lectin 1