{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:12:06Z","timestamp":1791295926240,"version":"4.1.0"},"reference-count":36,"publisher":"American Society for Microbiology","issue":"15","license":[{"start":{"date-parts":[[2012,8,1]],"date-time":"2012-08-01T00:00:00Z","timestamp":1343779200000},"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":[[2012,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>Recent studies in an experimental model of rabies showed major structural changes in the brain involving neuronal processes that are associated with severe clinical disease. Cultured adult rat dorsal root ganglion (DRG) neurons infected with the challenge virus standard-11 strain of rabies virus (CVS) showed axonal swellings and immunostaining for 4-hydroxy-2-nonenal (4-HNE), indicating evidence of lipid peroxidation associated with oxidative stress and reduced axonal growth compared to that of mock-infected DRG neurons. We have evaluated whether nuclear factor (NF)-\u03baB might act as a critical bridge linking CVS infection and oxidative stress. On Western immunoblotting, CVS infection induced expression of the NF-\u03baB p50 subunit compared to that of mock infection. Ciliary neurotrophic factor, a potent activator of NF-\u03baB, had no effect on mock-infected rat DRG neurons and reduced the number of 4-HNE-labeled puncta. SN50, a peptide inhibitor of NF-\u03baB, and CVS infection had an additive effect in producing axonal swellings, indicating that NF-\u03baB is neuroprotective. The fluorescent signal for subunit p50 was quantitatively evaluated in the nucleus and cytoplasm of mock- and CVS-infected rat DRG neurons. At 24 h postinfection (p.i.), there was a significant increase in the nucleus\/cytoplasm ratio, indicating increased transcriptional activity of NF-\u03baB, perhaps as a response to stress. At both 48 and 72 h p.i., there was significantly reduced nuclear localization of NF-\u03baB. CVS infection may induce oxidative stress by inhibiting nuclear activation of NF-\u03baB. A rabies virus protein may directly inhibit NF-\u03baB activity. Further investigations are needed to gain a better understanding of the basic mechanisms involved in the oxidative damage associated with rabies virus infection.<\/jats:p>","DOI":"10.1128\/jvi.00550-12","type":"journal-article","created":{"date-parts":[[2012,5,24]],"date-time":"2012-05-24T02:48:01Z","timestamp":1337827681000},"page":"8139-8146","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":21,"title":["Role of Nuclear Factor-\u03baB in Oxidative Stress Associated with Rabies Virus Infection of Adult Rat Dorsal Root Ganglion Neurons"],"prefix":"10.1128","volume":"86","author":[{"given":"Wafa","family":"Kammouni","sequence":"first","affiliation":[{"name":"Department of Internal Medicine (Neurology), University of Manitoba, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leena","family":"Hasan","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Neurology), University of Manitoba, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ali","family":"Saleh","sequence":"additional","affiliation":[{"name":"Division of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heidi","family":"Wood","sequence":"additional","affiliation":[{"name":"Zoonotic Diseases and Special Pathogens, Public Health Agency of Canada, Winnipeg, Manitoba, Canada"},{"name":"Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Fernyhough","sequence":"additional","affiliation":[{"name":"Division of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada"},{"name":"Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan C.","family":"Jackson","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Neurology), University of Manitoba, Winnipeg, Manitoba, Canada"},{"name":"Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/s12640-009-9074-5"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4798-06.2007"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.160027697"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awm199"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.48.4.881"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3127-04.2005"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1080\/13550280590900445"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(98)00214-7"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1941-08.2008"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.183434.111"},{"key":"e_1_3_2_12_2","first-page":"283","volume-title":"Rabies","author":"Iwasaki Y","year":"2002","unstructured":"IwasakiY TobitaM. 2002. 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