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Journal of Virology, February 2005, p. 1753-1764, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1753-1764.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Differential Induction of Antiviral Effects against West Nile Virus in Primary Mouse Macrophages Derived from Flavivirus-Susceptible and Congenic Resistant Mice by Alpha/Beta Interferon and Poly(I-C)

Ljiljana Pantelic,¹ Haran Sivakumaran,¹ and Nadezda Urosevic^1,2*

Microbiology, School of Biomedical and Chemical Sciences,¹ Western Australian Institute for Medical Research and University of Western Australia Centre for Medical Research, University of Western Australia, Crawley, Western Australia²

Received 15 April 2004/ Accepted 7 September 2004

A cell model of primary macrophages isolated from the peritoneal cavity of flavivirus-susceptible and congenic resistant mice has been used to study the extent and kinetics of antiviral effects against West Nile virus upon priming with alpha/beta interferon (IFN-/ß) or poly(I-C) (pIC). The pattern of flavivirus resistance expressed after priming of cells in this model was in good agreement with the pattern of flavivirus resistance described in the brains of the corresponding mouse strains. While priming with either IFN-/ß or pIC completely blocked flavivirus replication in macrophages from resistant mice, it only transiently reduced flavivirus replication in macrophages from susceptible mice. It was only the combined pretreatment with IFN-/ß and pIC that elicited strong antiviral responses that completely prevented flavivirus replication in macrophages from susceptible mice. Primary macrophages isolated from the blood of healthy human donors expressed a similar need for double-stranded RNA (dsRNA) cofactor in developing efficient antiviral responses against West Nile virus. These findings reveal that the inefficient IFN-/ß-induced antiviral effects against flaviviruses in cells from susceptible hosts could be successfully complemented by an external dsRNA factor leading to the complete eradication of the virus. This treatment appears to compensate for the lack of an inborn resistance mechanism in cells from the susceptible host. Furthermore, it may also provide useful clues for the prevention and treatment of flavivirus infections.

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* Corresponding author. Mailing address: Microbiology, School of Biomedical and Chemical Sciences, University of Western Australia, 35 Stirling Hwy., Crawley, Western Australia 6009. Phone: 61(8)-9346-2661. Fax: 61(8)-9346-2912. E-mail: nadia{at}cyllene.uwa.edu.au.

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Journal of Virology, February 2005, p. 1753-1764, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1753-1764.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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