{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:43:02Z","timestamp":1791420182313,"version":"4.3.3"},"reference-count":38,"publisher":"National Academy of Sciences","issue":"22","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2007,5,29]]},"abstract":"<jats:p>\n                    The poliovirus (PV) eradication campaign is conducted on the premise that this virus, because of the lack of a zoonotic reservoir, will not reemerge once eradicated. This report examines the origin of PV using theoretical and experimental approaches. Our rooted phylogenetic analysis suggests a speciation of PV from a C-cluster coxsackie A virus (C-CAV) ancestor through mutation of the capsid that caused a receptor switch from intercellular adhesion molecule-1 to CD155, leading to a change of pathogenicity. This hypothesis is supported experimentally with chimeras generated from three different pairs of PV and C-CAV. Those carrying the PV capsid and the replication proteins of C-CAVs replicated well, whereas their reciprocal counterparts were either debilitated or dead. This phenomenon of asymmetry is observed also in recombinants between PV1 and C-CAV20, selected in tissue culture cells using a previously undescribed protocol. The recombinants are generated at frequencies of 10\n                    <jats:sup>\u22126<\/jats:sup>\n                    typical for PV interserotype recombination. Strikingly, they resemble genetically and phenotypically, including neurovirulence in\n                    <jats:italic>CD155<\/jats:italic>\n                    transgenic mice, the large majority of circulating vaccine-derived PVs that have caused poliomyelitis outbreaks in different parts of the world. These data provide experimental evidence for C-CAVs being partners to PVs in generating diverse PV progeny by homologous recombination. They support speciation of a novel human pathogen (PV) from a pool of different human pathogens (C-CAVs). In a PV-free world without PV neutralizing antibodies, contemporary C-CAV, like their ancestor(s), could be fertile ground for a PV-like agent to emerge by mutation.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0700451104","type":"journal-article","created":{"date-parts":[[2007,5,22]],"date-time":"2007-05-22T18:08:20Z","timestamp":1179857300000},"page":"9457-9462","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":101,"title":["Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication"],"prefix":"10.1073","volume":"104","author":[{"given":"Ping","family":"Jiang","sequence":"first","affiliation":[{"name":"*Department of Molecular Genetics and Microbiology, School of Medicine, Stony Brook University, Stony Brook, NY 11794-5222; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johan A. J.","family":"Faase","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hidemi","family":"Toyoda","sequence":"additional","affiliation":[{"name":"*Department of Molecular Genetics and Microbiology, School of Medicine, Stony Brook University, Stony Brook, NY 11794-5222; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aniko","family":"Paul","sequence":"additional","affiliation":[{"name":"*Department of Molecular Genetics and Microbiology, School of Medicine, Stony Brook University, Stony Brook, NY 11794-5222; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eckard","family":"Wimmer","sequence":"additional","affiliation":[{"name":"*Department of Molecular Genetics and Microbiology, School of Medicine, Stony Brook University, Stony Brook, NY 11794-5222; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander E.","family":"Gorbalenya","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Leiden University Medical Center, 2300 RC, Leiden, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2007,5,29]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virusres.2005.04.008"},{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ge.27.120193.002033"},{"key":"e_1_3_4_3_2","first-page":"227","volume-title":"Molecular Biology of Picornaviruses","author":"Paul A","year":"2002","unstructured":"A Paul Molecular Biology of Picornaviruses, eds BL Semler, E Wimmer (Am Soc Microbiol Press, Washington, DC), pp. 227\u2013246 (2002)."},{"key":"e_1_3_4_4_2","first-page":"17","volume-title":"Molecular Biology of Picornaviruses","author":"Stanway G","year":"2002","unstructured":"G 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