Drak2 contributes to West Nile virus entry into the brain and lethal encephalitis

Shuhui Wang, Thomas Welte, Maureen McGargill, Terrence Town, Jesse Thompson, John F. Anderson, Richard A. Flavell, Erol Fikrig, Stephen M. Hedrick, Tian Wang

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

Death-associated protein kinase-related apoptosis-inducing kinase-2 (Drak2), a member of the death-associated protein family of serine/threonine kinases, is specifically expressed in T and B cells. In the absence of Drak2, mice are resistant to experimental autoimmune encephalomyelitis due to a decrease in the number of cells infiltrating the CNS. In the present study, we investigated the role of Drak2 in West Nile virus (WNV)-induced encephalitis and found that Drak2-/- mice were also more resistant to lethal WNV infection than wild-type mice. Although Drak2-/- mice had an increase in the number of IFN-γ-producing T cells in the spleen after infection, viral levels in the peripheral tissues were not significantly different between these two groups of mice. In contrast, there was a reduced viral load in the brains of Drak2-/- mice, which was accompanied by a decrease in the number of Drak2-/- CD4+ and CD8+ T cells in the brain following WNV infection. Moreover, we detected viral Ags in T cells isolated from the spleen or brain of WNV-infected mice. These results suggest that following a systemic infection, WNV might cross the blood brain barrier and enter the CNS by being carried by infected infiltrating T cells.

Original languageEnglish (US)
Pages (from-to)2084-2091
Number of pages8
JournalJournal of Immunology
Volume181
Issue number3
DOIs
StatePublished - Aug 1 2008
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Wang, S., Welte, T., McGargill, M., Town, T., Thompson, J., Anderson, J. F., Flavell, R. A., Fikrig, E., Hedrick, S. M., & Wang, T. (2008). Drak2 contributes to West Nile virus entry into the brain and lethal encephalitis. Journal of Immunology, 181(3), 2084-2091. https://doi.org/10.4049/jimmunol.181.3.2084