Respiratory syncytial virus inhibits interferon-α-inducible signaling in macrophage-like U937 cells

Abstract

Monocytes become susceptible to respiratory syncytial virus (RSV) infection when pretreated with phorbol 12-myristate 13-acetate (PMA). The molecular mechanism underlying this observation is poorly understood, but may be related to inhibition of type I interferon (IFN) signaling by RSV in epithelial cells. Herein, we have investigated the putative role of suppressor of cytokine signaling (SOCS) in the IFN-inducible antiviral response in U937 cells. Upon RSV infection of macrophage-like U937 cells, the expression of SOCS1, SOCS3, and CIS mRNA was rapidly upregulated, and phosphorylation of the IFN-alpha-inducible signal transducer and activator of transcription (STAT1 and STAT2) was suppressed. These results suggest that RSV can inhibit the phosphorylation of IFN-alpha-inducible STAT1 and STAT2 by inducing the expression of SOCS proteins in PMA-treated U937 cells.