{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T00:41:38Z","timestamp":1791074498658,"version":"4.1.0"},"reference-count":55,"publisher":"American Society for Microbiology","issue":"22","license":[{"start":{"date-parts":[[2008,11,15]],"date-time":"2008-11-15T00:00:00Z","timestamp":1226707200000},"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":[[2008,11,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>The B-cell response against West Nile virus (WNV), an encephalitic<jats:italic>Flavivirus<\/jats:italic>of global concern, is critical to controlling central nervous system dissemination and neurological sequelae, including death. Here, using a well-characterized mouse model of WNV infection, we examine the factors that govern early B-cell activation. Subcutaneous inoculation with a low dose of replicating WNV results in extensive B-cell activation in the draining lymph node (LN) within days of infection as judged by upregulation of the surface markers CD69, class II major histocompatibility complex, and CD86 on CD19<jats:sup>+<\/jats:sup>cells. B-cell activation in the LN but not the spleen was dependent on signals through the type I alpha\/beta interferon (IFN-\u03b1\/\u03b2) receptor. Despite significant activation in the draining LN at day 3 after infection, WNV-specific B cells were not detected by immunoglobulin M enzyme-linked immunospot analysis until day 7. Liposome depletion experiments demonstrate that B-cell activation after WNV infection was not affected by the loss of F4\/80<jats:sup>+<\/jats:sup>or CD169<jats:sup>+<\/jats:sup>subcapsular macrophages. Nonetheless, LN myeloid cells were essential for control of viral replication and survival from infection. Overall, our data suggest that the massive, early polyclonal B-cell activation occurring in the draining LN after WNV infection is immunoglobulin receptor and macrophage independent but requires sustained signals through the type I IFN-\u03b1\/\u03b2 receptor.<\/jats:p>","DOI":"10.1128\/jvi.01646-08","type":"journal-article","created":{"date-parts":[[2008,9,12]],"date-time":"2008-09-12T00:35:58Z","timestamp":1221179758000},"page":"10964-10974","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":75,"title":["Early B-Cell Activation after West Nile Virus Infection Requires Alpha\/Beta Interferon but Not Antigen Receptor Signaling"],"prefix":"10.1128","volume":"82","author":[{"given":"Whitney E.","family":"Purtha","sequence":"first","affiliation":[{"name":"Pathology &amp; Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen A.","family":"Chachu","sequence":"additional","affiliation":[{"name":"Pathology &amp; Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"IV","given":"Herbert W.","family":"Virgin","sequence":"additional","affiliation":[{"name":"Pathology &amp; Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S.","family":"Diamond","sequence":"additional","affiliation":[{"name":"Pathology &amp; Immunology"},{"name":"Medicine"},{"name":"Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80596-8"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/35099560"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.7.4635"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01718310"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1076071"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.13.6974-6981.2004"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.168.11.5716"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.0022-202x.2001.01454.x"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2007.06.007"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2004.08.007"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.3.1457"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0162-3109(99)00021-1"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.7.4343"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.0030106"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8456300"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.47.3.251"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.77.4.2578-2586.2003"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20031223"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid0704.017408"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1016\/0022-1759(92)90312-H"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200635993"},{"key":"e_1_3_2_23_2","doi-asserted-by":"crossref","first-page":"1710","DOI":"10.4049\/jimmunol.133.4.1710","volume":"133","year":"1984","unstructured":"Gerdes, J., H. 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