Swine and ruminant pestiviruses require the same cellular factor to enter bovine cells

• Published in: Journal of general virology 1996-06, Vol.77 (6), p.1295-1303
• Main Authors: Flores, Eduardo Furtado, Kreutz, Luiz C, Donis, Ruben O
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal; Border disease virus - physiology; Cattle; Cell Line; Cell Membrane - physiology; Cell Membrane - virology; Classical swine fever virus - physiology; Clone Cells; Disease Susceptibility; Endocytosis; Kidney; Mice; pestivirus; Pestivirus - physiology; Receptors, Virus - physiology; Sheep; Species Specificity; Swine
• ISSN: 0022-1317; 1465-2099
• DOI: 10.1099/0022-1317-77-6-1295

1 Department of Veterinary and Biomedical Sciences, University of Nebraska at Lincoln, Lincoln, NE 68583-0905 and 2 Swine Research Unit, National Animal Disease Center, USDA, PO Box 70, Ames, IA 50010, USA Pestiviruses initiate infection of susceptible cells by receptor-mediated endocytosis. Cellular plasma membrane or endosomal molecules involved in translocation of these viruses into the cytosol have not been unequivocally identified. We reported previously that a mutant cell line derived from Madin-Darby bovine kidney (MDBK) cells, termed CRIB-1, was resistant to infection with bovine viral diarrhoea virus. CRIB-1 cells were also resistant to infection with classical swine fever virus and border disease virus of sheep, suggesting that entry of these three different pestiviruses into bovine cells requires a common cell membrane function. The resistance is pestivirus-specific: CRIB-1 cells were as susceptible as the parental MDBK cells to 14 other viruses of cattle and swine belonging to unrelated families. The resistance of CRIB-1 cells to pestivirus infection involves a block in virus entry since transfection of virus RNA or virus inoculation in the presence of PEG resulted in productive infection. Furthermore, quantitative analyses of the outcome of PEG-mediated infection of CRIB-1 cells indicated that the intracellular milieu was fully permissive for pestivirus replication. Binding studies revealed that virus attachment to CRIB-1 cells was not completely abrogated. These results indicate that entry of pestiviruses into MDBK cells depends on a common plasma membrane or endosomal function, which is lacking in CRIB-1 cells. * Author for correspondence. Fax [phone]. e-mail [e-mail] Present address: Departamento de Medicina Veterinaria Preventiva, Universidade Federal de Santa Maria-UFSM, Santa Maria, RS, Brazil 97119. Received 13 November 1995; accepted 16 February 1996.