Despite the fact that the physiological function of interleukin-24 (IL-24) remains unknown, its pro-apoptotic activity, when expressed in an adenovirus background, is well documented, rendering IL-24 an attractive agent for anti-cancer-virotherapy. However, when used as a single agent, IL-24 only induces apoptosis in certain tumor cell lines. This work focuses on the oncolytic properties of an IL-24-expressing influenza A virus (delNS1/IL-24). The first part of the thesis revealed that the tumor-ablative activity of this chimeric influenza RNA virus induced cell death in cancer cells in an atypical, TLR3-associated death inducing signaling complex (TLR3-DISC) and caspase-8-dependent manner. Despite apoptosis is associated with the response to type I interferon the specific role of apoptosis as an antiviral mechanism has rarely been further investigated. As influenza A virus stimulates the TLR3 receptor, the second part of the thesis revealed, that IL-24 reduced the titer of this RNA virus in an apoptosis dependent manner. The antiviral effect could be blocked by a pan-caspase inhibitor, but also by siRNA directed towards TLR3. The induction of caspase-3 in virally infected and IL-24 treated cells was independent of type I IFN and correlated with a down-regulation of cFLIP and an activation of PKR and eIF2α, despite the later modulations appeared not to be sufficient for apoptosis induction. In conclusion, this work indicates, that i) the influenza A virus is an excellently suited vector to support the pro-apoptotic effect of IL-24 in cancer cells and that ii) interleukin-24 exerts an antiviral role within the immune response selectively purging virally infected, TLR3 stimulated cells. The data also suggests that apoptosis inducing cytokines and drugs might complement future antiviral strategies.