{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T04:58:58Z","timestamp":1791262738973,"version":"4.1.0"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2007,1,15]],"date-time":"2007-01-15T00:00:00Z","timestamp":1168819200000},"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":[[2007,1,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>The interferon-inducible adenosine deaminase that acts on double-stranded RNA (ADAR1-L) has been proposed to be one of the antiviral effector proteins within the complex innate immune response. Here, the potential role of ADAR1-L in the innate immune response to lymphocytic choriomeningitis virus (LCMV), a widely used virus model, was studied. Infection with LCMV clearly upregulated ADAR1-L expression and activity. The editing activity of ADAR1-L on an RNA substrate was not inhibited by LCMV replication. Accordingly, an adenosine-to-guanosine (A-to-G) and uracil-to-cytidine (U-to-C) hypermutation pattern was found in the LCMV genomic RNA in infected cell lines and in mice. In addition, two hypermutated clones with a high level of A-to-G or U-to-C mutations within a short stretch of the viral genome were isolated. Analysis of the functionality of viral glycoprotein revealed that A-to-G- and U-to-C-mutated LCMV genomes coded for nonfunctional glycoprotein at a surprisingly high frequency. Approximately half the GP clones with an amino acid mutation lacked functionality. These results suggest that ADAR1-L-induced mutations in the viral RNA lead to a loss of viral protein function and reduced viral infectivity. This study therefore provides strong support for the contribution of ADAR1-L to the innate antiviral immune response.<\/jats:p>","DOI":"10.1128\/jvi.00067-06","type":"journal-article","created":{"date-parts":[[2006,12,27]],"date-time":"2006-12-27T23:52:56Z","timestamp":1167263576000},"page":"457-464","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":66,"title":["A-to-G Hypermutation in the Genome of Lymphocytic Choriomeningitis Virus"],"prefix":"10.1128","volume":"81","author":[{"given":"Roland C.","family":"Zahn","sequence":"first","affiliation":[{"name":"Georg-Speyer-Haus, Institute for Biomedical Research, 60596 Frankfurt am Main, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ina","family":"Schelp","sequence":"additional","affiliation":[{"name":"Georg-Speyer-Haus, Institute for Biomedical Research, 60596 Frankfurt am Main, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olaf","family":"Utermo\u0308hlen","sequence":"additional","affiliation":[{"name":"Institute for Medical Microbiology, Immunology and Hygiene, Medical Center of the University of Cologne, 50935 Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorothee","family":"von Laer","sequence":"additional","affiliation":[{"name":"Georg-Speyer-Haus, Institute for Biomedical Research, 60596 Frankfurt am Main, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1101\/gr.7.8.843"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4400823"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.75.2.1061-1064.2001"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.77.5.2866-2872.2003"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.76.3.1488-1495.2002"},{"key":"e_1_3_2_7_2","first-page":"7","volume":"263","year":"2002","unstructured":"Biron, C. 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