{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:12:02Z","timestamp":1791295922153,"version":"4.1.0"},"reference-count":61,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2009,2,15]],"date-time":"2009-02-15T00:00:00Z","timestamp":1234656000000},"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":[[2009,2,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Gene expression of nonsegmented negative-strand RNA viruses is regulated at the transcriptional level and relies on the canonical 5\u2032-end-dependent translation of capped viral mRNAs. Here, we have used internal ribosome entry sites (IRES) from picornaviruses to control the expression level of the phosphoprotein P of the neurotropic rabies virus (RV;\n            <jats:italic>Rhabdoviridae<\/jats:italic>\n            ), which is critically required for both viral replication and escape from the host interferon response. In a dual luciferase reporter RV, the IRES elements of poliovirus (PV) and human rhinovirus type 2 (HRV2) were active in a variety of cell lines from different host species. While a generally lower activity of the HRV2 IRES was apparent compared to the PV IRES, specific deficits of the HRV2 IRES in neuronal cell lines were not observed. Recombinant RVs expressing P exclusively from a bicistronic nucleoprotein (N)-IRES-P mRNA showed IRES-specific reduction of replication in cell culture and in neurons of organotypic brain slice cultures, an increased activation of the beta interferon (IFN-\u03b2) promoter, and increased sensitivity to IFN. Intracerebral infection revealed a complete loss of virulence of both PV- and HRV2 IRES-controlled RV for wild-type mice and for transgenic mice lacking a functional IFN-\u03b1 receptor (IFNAR\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ). The virulence of HRV2 IRES-controlled RV was most severely attenuated and could be demonstrated only in newborn IFNAR\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice. Translational control of individual genes is a promising strategy to attenuate replication and virulence of live nonsegmented negative-strand RNA viruses and vectors and to study the function of IRES elements in detail.\n          <\/jats:p>","DOI":"10.1128\/jvi.02055-08","type":"journal-article","created":{"date-parts":[[2008,12,11]],"date-time":"2008-12-11T01:34:48Z","timestamp":1228959288000},"page":"1911-1919","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["Attenuation of Rabies Virus Replication and Virulence by Picornavirus Internal Ribosome Entry Site Elements"],"prefix":"10.1128","volume":"83","author":[{"given":"Adriane","family":"Marschalek","sequence":"first","affiliation":[{"name":"Max von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians-University, Feodor-Lynen-Str. 25, 81377 Munich"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Finke","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians-University, Feodor-Lynen-Str. 25, 81377 Munich"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Schwemmle","sequence":"additional","affiliation":[{"name":"Department of Virology, Institute for Medical Microbiology and Hygiene, Hermann-Herder-Strasse 11"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Mayer","sequence":"additional","affiliation":[{"name":"Department of Virology, Institute for Medical Microbiology and Hygiene, Hermann-Herder-Strasse 11"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernd","family":"Heimrich","sequence":"additional","affiliation":[{"name":"Institute of Anatomy and Cell Biology, Albertstr. 23, University of Freiburg, 79104 Freiburg"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lothar","family":"Stitz","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Friedrich-Loeffler-Institut Tu\u0308bingen, Paul-Ehrlich-Strasse 28, 72076 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl-Klaus","family":"Conzelmann","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer-Institute and Gene Center, Ludwig-Maximilians-University, Feodor-Lynen-Str. 25, 81377 Munich"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1125280"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0710650105"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2004.03.001"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virusres.2008.07.001"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5296-03.2004"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.3.1344-1351.2004"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.12.7673-7681.2005"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.80.6.2675-2683.2006"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.73.1.251-259.1999"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.10.6281-6290.2005"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.00714-06"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.vaccine.2008.08.069"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7536344"},{"key":"e_1_3_2_15_2","first-page":"1","volume":"283","year":"2004","unstructured":"Conzelmann, K. 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