{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:42:35Z","timestamp":1791286955597,"version":"4.1.0"},"reference-count":46,"publisher":"American Society for Microbiology","issue":"19","license":[{"start":{"date-parts":[[2006,10,1]],"date-time":"2006-10-01T00:00:00Z","timestamp":1159660800000},"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":[[2006,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>The\nemergence of West Nile virus (WNV) in the Western Hemisphere is marked\nby the spread of pathogenic lineage I strains, which differ from\ntypically avirulent lineage II strains. To begin to understand the\nvirus-host interactions that may influence the phenotypic properties of\ndivergent lineage I and II viruses, we compared the genetic,\npathogenic, and alpha\/beta interferon\n(IFN-\u03b1\/\u03b2)-regulatory properties of a lineage II isolate\nfrom Madagascar (MAD78) with those of a new lineage I isolate from\nTexas (TX02). Full genome sequence analysis revealed that MAD78\nclustered, albeit distantly, with other lineage II strains, while TX02\nclustered with emergent North American isolates, more specifically with\nother Texas strains. Compared to TX02, MAD78 replicated at low levels\nin cultured human cells, was highly sensitive to the antiviral actions\nof IFN in vitro, and demonstrated a completely avirulent phenotype in\nwild-type mice. In contrast to TX02 and other pathogenic forms of WNV,\nMAD78 was defective in its ability to disrupt IFN-induced JAK-STAT\nsignaling, including the activation of Tyk2 and downstream\nphosphorylation and nuclear translocation of STAT1 and STAT2. However,\nreplication of MAD78 was rescued in cells with a nonfunctional\nIFN-\u03b1\/\u03b2 receptor (IFNAR). Consistent with this finding,\nthe virulence of MAD78 was unmasked upon infection of mice lacking\nIFNAR. Thus, control of the innate host response and IFN actions is a\nkey feature of WNV pathogenesis and replication\nfitness.<\/jats:p>","DOI":"10.1128\/jvi.00768-06","type":"journal-article","created":{"date-parts":[[2006,9,14]],"date-time":"2006-09-14T03:35:27Z","timestamp":1158204927000},"page":"9424-9434","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":175,"title":["Resistance to Alpha\/Beta Interferon Is a Determinant of West Nile Virus Replication Fitness and Virulence"],"prefix":"10.1128","volume":"80","author":[{"given":"Brian C.","family":"Keller","sequence":"first","affiliation":[{"name":"Department\rof Microbiology, University of Texas Southwestern Medical Center,\rDallas, Texas 75390-9048"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brenda L.","family":"Fredericksen","sequence":"additional","affiliation":[{"name":"Department\rof Microbiology, University of Texas Southwestern Medical Center,\rDallas, Texas 75390-9048"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie A.","family":"Samuel","sequence":"additional","affiliation":[{"name":"Departments of\rMedicine and Molecular Microbiology, Washington University\rSchool of Medicine, St. Louis, Missouri\r63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard E.","family":"Mock","sequence":"additional","affiliation":[{"name":"Texas Veterinary Medical Diagnostic\rLaboratory, Amarillo, Texas 79116-3200"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter W.","family":"Mason","sequence":"additional","affiliation":[{"name":"Department of\rPathology, University of Texas Medical Branch, Galveston,\rTexas 77555-0436"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S.","family":"Diamond","sequence":"additional","affiliation":[{"name":"Departments of\rMedicine and Molecular Microbiology, Washington University\rSchool of Medicine, St. Louis, Missouri\r63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"Michael","family":"Gale","sequence":"additional","affiliation":[{"name":"Department\rof Microbiology, University of Texas Southwestern Medical Center,\rDallas, Texas 75390-9048"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"1","volume":"28","year":"1996","unstructured":"Adachi, J., and M. 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