Sendai virus (SeV) leader (le) and trailer (tr) RNAs are short transcripts generated during abortive antigenome and genome synthesis, respectively. Recom binant SeV (rSeV) that express tr‐like RNAs from the leader region are non‐cytopathic and, moreover, prevent wild‐type SeV from inducing apoptosis in mixed infections. These rSeV thus appear to have gained a function. Here we report that tr RNA binds to a cellular protein with many links to apoptosis (TIAR) via the AU‐rich sequence 5′ UUUUAAAUUUU. Duplication of this AU‐rich sequence alone within the le RNA confers TIAR binding on this le* RNA and a non‐cytopathic phenotype to these rSeV in cell culture. Transgenic overexpression of TIAR during SeV infection promotes apoptosis and reverses the anti‐apoptotic effects of le* RNA expression. More over, TIAR overexpression and SeV infection act synergistically to induce apoptosis. These short viral RNAs may act by sequestering TIAR, a multivalent RNA recognition motif (RRM) family RNA‐binding protein involved in SeV‐induced apoptosis. In this view, tr RNA is not simply a by‐product of abortive genome synthesis, but is also an antigenome transcript that modulates the cellular antiviral response.