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To successfully infect a host, a virus must overcome this blockage by either controlling eIF2\u03b1 phosphorylation or by utilizing a noncanonical mode of translation initiation. Here we show that enterovirus RNA is sensitive to translation inhibition resulting from eIF2\u03b1 phosphorylation, but it becomes resistant as infection progresses. Further, we show that the cleavage of initiation factor eIF5B during enteroviral infection, along with the viral internal ribosome entry site, plays a role in mediating viral translation under conditions that are nonpermissive for host cell translation. Together, these results provide a mechanism by which enteroviruses evade the antiviral response and provide insight into a noncanonical mechanism of translation initiation.<\/jats:p>","DOI":"10.1128\/jvi.00792-11","type":"journal-article","created":{"date-parts":[[2011,6,23]],"date-time":"2011-06-23T06:43:42Z","timestamp":1308811422000},"page":"8884-8893","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["Poliovirus Switches to an eIF2-Independent Mode of Translation during Infection"],"prefix":"10.1128","volume":"85","author":[{"given":"James P.","family":"White","sequence":"first","affiliation":[{"name":"Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucas C.","family":"Reineke","sequence":"additional","affiliation":[{"name":"Department of Molecular Virology and 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