As part of their pathogenic life cycle, picornaviruses have evolved specific genetic elements (internal ribosomal entry sites; IRES) in their 5 nontranslated leader regions (ntr) which adopt a particular secondary structure able to attract eukaryotic ribosomes and to allow internal translation-initiation (Belsham and Sonenberg, 1996 ; Table 1 ). The pivotal role of IRES in picornaviral pathogenesis is based on the expression of a viral protease which cleaves the host cap-binding translation-initiation factor eIF4G and allows redirection of host translation machinery for exclusive translation-initiation of IRES-containing viral mRNAs (Etchison et al., 1982; Pelletier and Sonenberg, 1988; Jackson et al., 1990; Belsham and Sonenberg, 1996; Rueckert, 1996) .