This thesis describes that RNA silencing suppressor (RSS) proteins encoded by negative-stranded RNA plant viruses are able to interfere with different RNA silencing pathways in a variety of organisms by interacting with double stranded (ds)RNA molecules. These RSS proteins are able to counteract the antiviral RNA silencing response in their plant host and insect vector, and even in mammalian cells, that are non-hosts for these viruses. Whereas Rice hoja blanca virus NS3 has been shown to bind size specific dsRNA, most tospovirus NSs proteins, in contrast, bind dsRNA size-independently and thus are able to interfere at two different stages in the RNA silencing pathway: RNA-induced silencing complex assembly and in Dicer cleavage. In addition to the interaction with the antiviral small interfering (si)RNA pathway both RSS proteins were able to interfere with the micro (mi)RNA pathway, which is important for host gene regulation. This is probably due to the structural similarities among the dsRNA molecules (siRNA and miRNA/miRNA* duplexes). Computer prediction supports the idea that the miRNA pathway (or at least certain miRNA/miRNA* duplexes) could potentially act as antiviral response in insects and plants, as recently reported for mammals. Furthermore, the ability of NS3 to trans-complement HIV-1 for the proposed HIV-1 RSS, the Tat protein, and restore virus production at wild type virus levels, supports the recent observation that at least certain mammalian-infecting viruses are restricted by small dsRNA molecules and highlights the use of well characterized plant RSS proteins as tool to study viral counter defense in a variety of eukaryotic systems.