{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T16:43:34Z","timestamp":1791132214332,"version":"4.1.0"},"reference-count":45,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2010,6,15]],"date-time":"2010-06-15T00:00:00Z","timestamp":1276560000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2010,6,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Poliovirus (PV) 2A\n            <jats:sup>pro<\/jats:sup>\n            has been considered important for PV replication and is known to be toxic to host cells. A 2A\n            <jats:sup>pro<\/jats:sup>\n            -deficient PV would potentially be less toxic and ideal as a vector. To examine whether 2A\n            <jats:sup>pro<\/jats:sup>\n            is needed to form progeny virus, a full-length cDNA of dicistronic (\n            <jats:italic>dc<\/jats:italic>\n            ) PV with (pOME) or without (pOME\u03942A) 2A\n            <jats:sup>pro<\/jats:sup>\n            was constructed in the strain PV1(M)OM. RNAs of both pOME and pOME\u03942A were capable of forming progeny viruses, called OME and OME\u03942A, respectively. In their ability to induce a cytopathic effect (CPE), the strains ranked as OME\u03942A &lt; OME \u2252 PV1(M)OM. These results suggest that 2A\n            <jats:sup>pro<\/jats:sup>\n            is not essential for full-length\n            <jats:italic>dc<\/jats:italic>\n            PV to form progeny virus and that it contributes to the efficient viral replication and\/or induction of a CPE. To clarify whether 2A\n            <jats:sup>pro<\/jats:sup>\n            is essential for P1-null (lacking the entire coding sequence for capsid proteins) PV, the RNA replication activity of P1-null PV (pOM\u0394P1) or P1-null PV without 2A\n            <jats:sup>pro<\/jats:sup>\n            (pOM\u0394P1\u03942A) or without both 2A\n            <jats:sup>pro<\/jats:sup>\n            and 2B (pOM\u0394P1\u03942A\u03942B) was examined. The RNAs of pOM\u0394P1 and pOM\u0394P1\u03942A could replicate and form progeny viruses under a\n            <jats:italic>trans<\/jats:italic>\n            supply of P1 protein, whereas the RNA of pOM\u0394P1\u03942A\u03942B could not. These results suggest that 2A\n            <jats:sup>pro<\/jats:sup>\n            is not needed for the replication of P1-null PV, although it is important for PV RNA replication and inducing a CPE. To know whether a 2A\n            <jats:sup>pro<\/jats:sup>\n            -deficient PV can be used as a vector, a P1-null PV containing the enhanced green fluorescent protein (EGFP) coding sequence with or without 2A\n            <jats:sup>pro<\/jats:sup>\n            was examined. It expressed fluorescent protein. This result suggests that 2A\n            <jats:sup>pro<\/jats:sup>\n            -deficient PV can express foreign genes.\n          <\/jats:p>","DOI":"10.1128\/jvi.02575-09","type":"journal-article","created":{"date-parts":[[2010,4,15]],"date-time":"2010-04-15T01:34:58Z","timestamp":1271295298000},"page":"5947-5957","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":14,"title":["2A Protease Is Not a Prerequisite for Poliovirus Replication"],"prefix":"10.1128","volume":"84","author":[{"given":"Hiroko","family":"Igarashi","sequence":"first","affiliation":[{"name":"Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuko","family":"Yoshino","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miwako","family":"Miyazawa","sequence":"additional","affiliation":[{"name":"Japan Poliomyelitis Research Institute, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hitoshi","family":"Horie","sequence":"additional","affiliation":[{"name":"Japan Poliomyelitis Research Institute, Tokyo, Japan"},{"name":"Department of Microbiology, Faculty of Pharmaceutical Science, Ohu University, Fukushima, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seii","family":"Ohka","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akio","family":"Nomoto","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1998.9438"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.12.5534-5541.2000"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1535607"},{"key":"e_1_3_2_5_2","first-page":"6359","volume":"54","year":"1994","unstructured":"Ansardi, D. 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