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

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.

journal_name

J Virol

journal_title

Journal of virology

authors

Rahbar R,Murooka TT,Hinek AA,Galligan CL,Sassano A,Yu C,Srivastava K,Platanias LC,Fish EN

doi

10.1128/JVI.00463-06

subject

Has Abstract

pub_date

2006-07-01 00:00:00

pages

7245-59

issue

14

eissn

0022-538X

issn

1098-5514

pii

80/14/7245

journal_volume

80

pub_type

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