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Virology. 2010 Jan 5;396(1):30-6. doi: 10.1016/j.virol.2009.10.019. Epub 2009 Nov 7.

JNK phosphorylation, induced during dengue virus infection, is important for viral infection and requires the presence of cholesterol.

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1
Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del IPN, Av. IPN 2508. Col. San Pedro Zacatenco, México City, D.F. C.P. 07360, México.

Abstract

Infection with a broad diversity of viruses often activates host cell signaling pathways including the mitogen-activated protein kinase pathway. The present study established that dengue virus infection of human macrophages activates Jun NH(2)-terminal kinase (JNK) and the p38 MAPKs pathways. The activation was observed at early times after infection and occurs when either infectious or UV-inactivated dengue virus was used. The role of these activated kinases in dengue virus infection was evaluated using specific inhibitors. Inhibition of JNK and p38 kinases did result in a significant reduction in viral protein synthesis and in viral yield. Additionally, lipid rafts disruption induced a strong inhibition of JNK activation. These results suggest that, at early stages after dengue virus infection, MAPKs are activated and that activation of JNK and p38 is required for dengue virus infection.

PMID:
19897220
DOI:
10.1016/j.virol.2009.10.019
[Indexed for MEDLINE]
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