Our early use of microarrays also included the first systematic attempt to define the full repertoire of dsRNA-regulated genes [4] , and we used arrays, in conjunction with polysome fractionation, to identify cellular and viral mRNAs that increased in abundance and which were selectively recruited to polyribosomes following influenza virus infection [5] . Our dsRNA study identified 175 dsRNA-stimulated genes, which encoded proteins involved in a broad range of cellular functions and metabolic pathways. In addition, this study showed for the first time that many genes are also down-regulated by dsRNA. Our polysome fractionation studies, headed by John Kash, revealed that many of the cellular mRNAs that are recruited to polyribosomes during influenza virus infection are involved in the control of cell proliferation and survival, mitogenesis, or the inflammatory response. In addition, many of these mRNAs contain a putative binding site for GRSF-1, a cellular mRNA-binding protein that also specifically interacts with a discrete and conserved region of the viral 5′ untranslated region [6] .