Vaccinia virus activation of CCR5 invokes tyrosine phosphorylation signaling events that support virus replication

Ramtin Rahbar, Thomas T. Murooka, Anna A. Hinek, Carole L. Galligan, Antonella Sassano, Celeste Yu, Kishore Srivastava, Leonidas C. Platanias, Eleanor N. Fish*

*Corresponding author for this work

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Vaccinia virus, a poxvirus, produces structurally distinct forms of virions for which the immediate events following cell entry are ill-defined. We provide evidence that intracellular mature virus (IMV) enters both permissive and nonpermissive T-cell lines and that introduction of CCR5 into nonpermissive mouse fibroblasts or human primary T cells renders the cells permissive for vaccinia replication. Notably, T cells expressing CCR5 in which tyrosine 339 in the intracellular region is replaced by phenylalanine no longer support virus replication or virus-inducible activation of specific host cell signaling effectors IRS-2, Grb2, and Erk1/2. We show that following IMV entry into the cell, the intact but not the tyrosine-deficient CCR5 is rapidly internalized and colocalizes with virus. This colocalization precedes virus-inducible signaling and replication.

Original languageEnglish (US)
Pages (from-to)7245-7259
Number of pages15
JournalJournal of virology
Volume80
Issue number14
DOIs
StatePublished - Jul 1 2006

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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    Rahbar, R., Murooka, T. T., Hinek, A. A., Galligan, C. L., Sassano, A., Yu, C., Srivastava, K., Platanias, L. C., & Fish, E. N. (2006). Vaccinia virus activation of CCR5 invokes tyrosine phosphorylation signaling events that support virus replication. Journal of virology, 80(14), 7245-7259. https://doi.org/10.1128/JVI.00463-06