Fig 10.

WEEV structural proteins inhibit neuronal antiviral PRR signaling in neurons at a step downstream of IRF-3 activation. (A) BE(2)-C/m ISRE promoter-reporter cells were cotransfected with a control HA-tagged β-galactosidase (β-gal) expression vector, a second vector containing no insert (empty vector control) or encoding a dominant negative IRF-3 (dnIRF-3) or the WEEV nsP1, capsid (Cap), or capsid-envelope (Cap-Env) protein, and a third vector encoding the indicated superactive (sa) or wild-type PRR-pathway component. Reporter gene activity was measured 48 h after transfection, and results are expressed relative to empty vector transfected controls (dashed line). *, P ≤ 0.05. (B) Lysates from the transfected cells described in panel A were analyzed by immunoblotting for TRIF, MDA5, IRF-3, HA-tagged β-gal, and GAPDH as a loading control.