The amino acid sequences of GII. 4.1987 , GII.4.2002 , and GII.4.2006 capsids were individually aligned to the VA387 P domain sequence using Clustalx1.86 [78] , and the GII.4.2002 domain dimer X-ray crystal structure (PDB accession: 2OBT) [16] was used as a template for generating homology models. Homology models were generated using the program Modeller available via the Max Planck Institute Bioinformatics Toolkit (http://toolkit.tuebingen.mpg.de/). The structural models were analyzed and compared, and figures were generated using Mac Pymol (Delano Scientific).  Induction of GADD34 Is Necessary for dsRNA-Dependent Interferon-β Production and Participates in the Control of Chikungunya Virus Infection Nucleic acid sensing by cells is a key feature of antiviral responses, which generally result in type-I Interferon production and tissue protection. However, detection of double-stranded RNAs in virus-infected cells promotes two concomitant and apparently conflicting events. The dsRNA-dependent protein kinase (PKR) phosphorylates translation initiation factor 2-alpha (eIF2α) and inhibits protein synthesis, whereas cytosolic DExD/H box RNA helicases induce expression of type I-IFN and other cytokines. We demonstrate that the phosphatase-1 cofactor, growth arrest and DNA damage-inducible protein 34 (GADD34/Ppp1r15a), an important component of the unfolded protein response (UPR), is absolutely required for type I-IFN and IL-6 production by mouse embryonic fibroblasts (MEFs) in response to dsRNA. GADD34 expression in MEFs is dependent on PKR activation, linking cytosolic microbial sensing with the ATF4 branch of the UPR. The importance of this link for anti-viral immunity is underlined by the extreme susceptibility of GADD34-deficient fibroblasts and neonate mice to Chikungunya virus infection. During their replication in host cells, RNA and DNA viruses generate RNA intermediates, which elicit antiviral responses mostly through type-I interferon (IFN) production [1, 2] . Several families of proteins are known to sense double-stranded RNA (dsRNA), including endocytic Toll-like receptor 3 (TLR3) [3] , the dsRNA-dependent protein kinase (PKR) [4] and the interferoninducible 29-59-oligoadenylates and endoribonuclease L system (OAS/2-5A/RNase L) [5] . Viral dsRNA and the synthetic dsRNA analog polyriboinosinic:polyribocytidylic acid (poly I:C) are also detected by different cytosolic DExD/H box RNA helicases such as the melanoma differentiation-associated gene 5 (MDA5), DDX1, DDX21, and DHX36, which, once activated, trigger indirectly the phosphorylation and the nuclear translocation of transcription factors such as IRF-3 and IRF-7, resulting predominantly in abundant type-I IFN and pro-inflammatory cytokines production by the infected cells [1, 6, 7] .