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In addition, P is an essential cofactor of the viral polymerase and is required for encapsidation of viral RNA into nucleoprotein during replication. By site-directed mutagenesis, we have identified a domain of P required for efficient inhibition of IFN induction. Phosphoproteins lacking amino acids (aa) 176 to 181, 182 to 186, or 176 to 186 were severely compromised in counteracting phosphorylation of IRF3 and IRF7 by TBK1 or IKKi while retaining the full capacity of preventing nuclear import of activated STATs and of supporting virus transcription and replication. Recombinant RV carrying the mutated phosphoproteins (the SAD \u0394Ind1, SAD \u0394Ind2, and SAD \u0394Ind1\/2 viruses) activated IRF3 and beta IFN (IFN-\u03b2) transcription in infected cells but still blocked STAT-mediated expression of IFN-stimulated genes. Due to a somewhat higher transcription rate, the SAD \u0394Ind1 virus activated IRF3 more efficiently than the SAD \u0394Ind2 virus. After intracerebral injection into mouse brains at high doses, the SAD \u0394Ind1 virus was completely apathogenic for wild-type (wt) mice, while the SAD \u0394Ind2 virus was partially attenuated and caused a slower progression of lethal rabies than wt RV. Neurovirulence of IFN-resistant RV thus correlates with the capacity of the virus to prevent activation of IRF3 and IRF7.<\/jats:p>","DOI":"10.1128\/jvi.01427-10","type":"journal-article","created":{"date-parts":[[2010,11,18]],"date-time":"2010-11-18T03:27:16Z","timestamp":1290050836000},"page":"842-852","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":92,"title":["Genetic Dissection of Interferon-Antagonistic Functions of Rabies Virus Phosphoprotein: Inhibition of Interferon Regulatory Factor 3 Activation Is Important for Pathogenicity"],"prefix":"10.1128","volume":"85","author":[{"given":"Martina","family":"Rieder","sequence":"first","affiliation":[{"name":"Max von Pettenkofer Institute &amp; Gene Center, Ludwig Maximilians University, D-81377 Mu\u0308nchen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krzysztof","family":"Brzo\u0301zka","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer Institute &amp; Gene Center, Ludwig Maximilians University, D-81377 Mu\u0308nchen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian K.","family":"Pfaller","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer Institute &amp; Gene Center, Ludwig Maximilians University, D-81377 Mu\u0308nchen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James H.","family":"Cox","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Friedrich Loeffler Institute, D-72076 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lothar","family":"Stitz","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Friedrich Loeffler Institute, D-72076 Tu\u0308bingen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl-Klaus","family":"Conzelmann","sequence":"additional","affiliation":[{"name":"Max von Pettenkofer Institute &amp; Gene Center, Ludwig Maximilians University, D-81377 Mu\u0308nchen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gene.6364449"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205931"},{"key":"e_1_3_2_4_2","first-page":"211","year":"2009","unstructured":"Brz\u00f3zka, K., and K. 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