During pathogenesis, viruses hijack the cellular machinery to access molecules and sub-cellular structures needed for infection. Viruses counteract plant defences by producing suppressor proteins. We have evidence that multifunctional viral protein—translation transactivator/ viroplasmin from Cauliflower mosaic virus, CaMV—could be used as a suppressor of cellular RNA turnover: the cellular accumulation of TAV inhibits cellular mRNA decay and suggests its complex formation with the decapping machinery within P-bodies.We shall investigate whether TAV of CaMV and related pararetroviruses serves as a suppressor of cellular and viral RNA degradation, and whether TAV is operated within either the deadenylation complex, which primes mRNA degradation, and/or the decapping complex, where TAV integrates. We shall test whether transient or stable over-expression of the CaMV TAV as a wild type or a mutant form is able to suppress degradation of cellular or viral RNAs. We shall determine the component of the degradation machinery that ensures TAV entry into the decapping complex/ P-bodies. Thus, we are interesting in studying the TAV interaction network within the decapping/ deadenylation complexes.These studies should reveal whether viral protein-based suppression of RNA degradation is a universal mechanism employed by plant pararetroviruses and, perhaps, also animal retroviruses. Additionally we shall identify RNA-based targets within cellular and viral mRNAs, and study whether synergistic suppression of RNA degradation by viral suppressor might contribute to CaMV virulence. This will help to design new strategies to counteract mRNA degradation in general using plant pararetroviral vector.