Volume 17, Issue 3, Pages 287-289 (March 2015) Caps Off to Poxviruses  Robert H. Silverman  Cell Host & Microbe  Volume 17, Issue 3, Pages 287-289 (March 2015) DOI: 10.1016/j.chom.2015.02.013 Copyright © 2015 Elsevier Inc. Terms and Conditions

Figure 1 Poxviruses Antagonize Antiviral Innate Immunity by Limiting the Accumulation of DsRNA Late in the vaccinia virus (VACV) replication cycle, complementary, converging viral transcripts anneal to form dsRNA. However, accumulation of viral dsRNA is limited due to the combined activities of two viral mRNA decapping enzymes (D9 and D10) and the host 5′-to-3′ exoribonuclease Xrn1. When D9 and D10 are mutated in the same virus, or when Xrn1 is depleted with RNAi, viral dsRNA accumulates to high levels activating the host antiviral proteins OAS and PKR. OAS produces 2-5A, which activates RNase L, causing degradation of viral RNA and rRNA, whereas PKR phosphorylates eIF2α. Both pathways inhibit protein synthesis, thus preventing viral replication. The VACV E3L gene encodes two dsRNA binding proteins that reduce PKR and OAS activation. Modified from McFadden (2005). Cell Host & Microbe 2015 17, 287-289DOI: (10.1016/j.chom.2015.02.013) Copyright © 2015 Elsevier Inc. Terms and Conditions