Open Access Research

Identification of the ovine mannose receptor and its possible role in Visna/Maedi virus infection

Helena Crespo1, Ramsés Reina1, Idoia Glaria1, Hugo Ramírez14, Ximena de Andrés1, Paula Jáuregui1, Lluís Luján2, Luisa Martínez-Pomares3, Beatriz Amorena1 and Damián F de Andrés1*

  • * Corresponding author: Damián F de Andrés ancad@unavarra.es

  • † Equal contributors

Author Affiliations

1 Institute of Agrobiotechnology, CSIC-UPNA-Government of Navarra, Ctra Mutilva, 31192 Mutilva, Spain

2 Department of Animal Pathology, University of Zaragoza, Miguel Servet 177, 50013 Zaragoza, Spain

3 School of Molecular Medical Sciences, University of Nottingham, Queen's Medical Centre, Floor A, West Block, Room 1323, Nottingham NG7 2UH, UK

4 Laboratory of Virology, Genetics and Molecular Biology. FESC, UNAM. C-4, 54700 Cuautitlán Izcalli, State of Mexico, Mexico

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Veterinary Research 2011, 42:28  doi:10.1186/1297-9716-42-28

Published: 7 February 2011

Abstract

This study aims to characterize the mannose receptor (MR) gene in sheep and its role in ovine visna/maedi virus (VMV) infection. The deduced amino acid sequence of ovine MR was compatible with a transmembrane protein having a cysteine-rich ricin-type amino-terminal region, a fibronectin type II repeat, eight tandem C-type lectin carbohydrate-recognition domains (CRD), a transmembrane region, and a cytoplasmic carboxy-terminal tail. The ovine and bovine MR sequences were closer to each other compared to human or swine MR. Concanavalin A (ConA) inhibited VMV productive infection, which was restored by mannan totally in ovine skin fibroblasts (OSF) and partially in blood monocyte-derived macrophages (BMDM), suggesting the involvement of mannosylated residues of the VMV ENV protein in the process. ConA impaired also syncytium formation in OSF transfected with an ENV-encoding pN3-plasmid. MR transcripts were found in two common SRLV targets, BMDM and synovial membrane (GSM) cells, but not in OSF. Viral infection of BMDM and especially GSM cells was inhibited by mannan, strongly suggesting that in these cells the MR is an important route of infection involving VMV Env mannosylated residues. Thus, at least three patterns of viral entry into SRLV-target cells can be proposed, involving mainly MR in GSM cells (target in SRLV-induced arthritis), MR in addition to an alternative route in BMDM (target in SRLV infections), and an alternative route excluding MR in OSF (target in cell culture). Different routes of SRLV infection may thus coexist related to the involvement of MR differential expression.