{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T13:17:37Z","timestamp":1781011057172,"version":"3.54.1"},"reference-count":36,"publisher":"American Society for Microbiology","issue":"17","license":[{"start":{"date-parts":[[2003,9,1]],"date-time":"2003-09-01T00:00:00Z","timestamp":1062374400000},"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":[[2003,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Rubella virus (RUB) replicons with an in-frame deletion of 507 nucleotides between two\n            <jats:italic>Not<\/jats:italic>\n            I sites in the P150 nonstructural protein (\u0394\n            <jats:italic>Not<\/jats:italic>\n            I) do not replicate (as detected by expression of a reporter gene encoded by the replicon) but can be amplified by wild-type helper virus (Tzeng et al., Virology\n            <jats:bold>289:<\/jats:bold>\n            63-73, 2001). Surprisingly, virus with \u0394\n            <jats:italic>Not<\/jats:italic>\n            I was viable, and it was hypothesized that this was due to complementation of the\n            <jats:italic>Not<\/jats:italic>\n            I deletion by one of the virion structural protein genes. Introduction of the capsid (C) protein gene into \u0394\n            <jats:italic>Not<\/jats:italic>\n            I-containing replicons as an in-frame fusion with a reporter gene or cotransfection with both \u0394\n            <jats:italic>Not<\/jats:italic>\n            I replicons and RUB replicon or plasmid constructs containing the C gene resulted in replication of the \u0394\n            <jats:italic>Not<\/jats:italic>\n            I replicon, confirming the hypothesis that the C gene was the structural protein gene responsible for complementation and demonstrating that complementation could occur either in\n            <jats:italic>cis<\/jats:italic>\n            or in\n            <jats:italic>trans<\/jats:italic>\n            . Approximately the 5\u2032 one-third of the C gene was necessary for complementation. Mutations that prevented translation of the C protein while minimally disturbing the C gene sequence abrogated complementation, while synonymous codon mutations that changed the C gene sequence without affecting the amino acid sequence at the 5\u2032 end of the C gene had no effect on complementation, indicating that the C protein, not the C gene RNA, was the moiety responsible for complementation. Complementation occurred at a basic step in the virus replication cycle, because \u0394\n            <jats:italic>Not<\/jats:italic>\n            I replicons failed to accumulate detectable virus-specific RNA.\n          <\/jats:p>","DOI":"10.1128\/jvi.77.17.9502-9510.2003","type":"journal-article","created":{"date-parts":[[2003,8,14]],"date-time":"2003-08-14T22:53:50Z","timestamp":1060901630000},"page":"9502-9510","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":40,"title":["Complementation of a Deletion in the Rubella Virus P150 Nonstructural Protein by the Viral Capsid Protein"],"prefix":"10.1128","volume":"77","author":[{"given":"Wen-Pin","family":"Tzeng","sequence":"first","affiliation":[{"name":"Department of Biology, Georgia State University, Atlanta, Georgia 30302-4010"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teryl K.","family":"Frey","sequence":"additional","affiliation":[{"name":"Department of Biology, Georgia State University, Atlanta, Georgia 30302-4010"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","unstructured":"Adams S. 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