{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T17:04:44Z","timestamp":1790874284997,"version":"4.1.0"},"reference-count":28,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2002,5,15]],"date-time":"2002-05-15T00:00:00Z","timestamp":1021420800000},"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":[[2002,5,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            In studies of acute hepatitis C virus (HCV) infection, the early host immune response is one of the determinants of viral persistence. The class I human leukocyte antigens (HLA), which present foreign antigen to cytolytic T cells, are integral components of this response. We hypothesized that the highly polymorphic\n            <jats:italic>HLA<\/jats:italic>\n            genes affect the outcome of an HCV infection. To test this hypothesis, we molecularly typed 231 persons with well-documented clearance of an HCV infection and 444 matched persistently infected persons.\n            <jats:italic>HLA-A*1101<\/jats:italic>\n            (odds ratio [OR], 0.49; 95% confidence interval [95% CI], 0.27 to 0.89),\n            <jats:italic>HLA-B*57<\/jats:italic>\n            (OR, 0.62; 95% CI, 0.39 to 1.00), and\n            <jats:italic>HLA-Cw*0102<\/jats:italic>\n            (OR, 0.43; 95% CI, 0.21 to 0.89) were associated with viral clearance, whereas\n            <jats:italic>HLA-A*2301<\/jats:italic>\n            (OR, 1.78; 95% CI, 1.01 to 3.11) and\n            <jats:italic>HLA-Cw*04<\/jats:italic>\n            (OR, 1.78; 95% CI, 1.21 to 2.59) were associated with viral persistence.\n            <jats:italic>HLA-Cw*04<\/jats:italic>\n            is in strong linkage disequilibrium with\n            <jats:italic>HLA-B*53<\/jats:italic>\n            and\n            <jats:italic>HLA-B*35<\/jats:italic>\n            , but only\n            <jats:italic>HLA-B*53<\/jats:italic>\n            (OR, 1.70; 95% CI, 0.95 to 3.06) and the\n            <jats:italic>Cw*04-B*53<\/jats:italic>\n            haplotype (OR, 1.76; 95% CI, 0.94 to 3.26) were weakly associated with viral persistence.\n            <jats:italic>HLA-B*53<\/jats:italic>\n            has similar, but not necessarily identical, binding specificity to some\n            <jats:italic>HLA-B*35<\/jats:italic>\n            subtypes (\n            <jats:italic>B*35-Px<\/jats:italic>\n            group). The association with the\n            <jats:italic>B*35-Px<\/jats:italic>\n            group was less strong than with\n            <jats:italic>HLA-B*53<\/jats:italic>\n            alone. The association of\n            <jats:italic>HLA-Cw*04<\/jats:italic>\n            with HCV persistence was codominant (two copies of the gene were more strongly associated with persistence than one copy). However,\n            <jats:italic>HLA-Cw*04<\/jats:italic>\n            was not associated with HCV RNA levels among the persistently infected individuals. Since Cw*04 is a ligand for the killer immunoglobulin-like receptors on natural killer cells, these cells may be involved in recovery from HCV infection. Further investigation is needed to understand the relationship between class I alleles and HCV clearance.\n          <\/jats:p>","DOI":"10.1128\/jvi.76.10.4792-4797.2002","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:09:29Z","timestamp":1027764569000},"page":"4792-4797","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":140,"title":["<i>HLA-Cw*04<\/i>\n            and Hepatitis C Virus Persistence"],"prefix":"10.1128","volume":"76","author":[{"given":"Chloe L.","family":"Thio","sequence":"first","affiliation":[{"name":"Department of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaojiang","family":"Gao","sequence":"additional","affiliation":[{"name":"Laboratory of Genomic Diversity, National Cancer Institute, Frederick"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James J.","family":"Goedert","sequence":"additional","affiliation":[{"name":"Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Vlahov","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Medical Institutions, Baltimore"},{"name":"New York Academy of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenrad E.","family":"Nelson","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Johns Hopkins Medical Institutions, Baltimore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret W.","family":"Hilgartner","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, New York Presbyterian Hospital-Cornell Medical Center, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen J.","family":"O'Brien","sequence":"additional","affiliation":[{"name":"Laboratory of Genomic Diversity, National Cancer Institute, Frederick"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Karacki","sequence":"additional","affiliation":[{"name":"Department of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacquie","family":"Astemborski","sequence":"additional","affiliation":[{"name":"Department of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary","family":"Carrington","sequence":"additional","affiliation":[{"name":"Laboratory of Genomic Diversity, National Cancer Institute, Frederick"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David L.","family":"Thomas","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Epidemiology, Johns Hopkins Medical Institutions, Baltimore"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.510260701"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(95)00039-X"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8278(99)80249-9"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.283.5408.1748"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80065-5"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80044-8"},{"key":"e_1_3_2_8_2","first-page":"451","volume":"109","year":"1997","unstructured":"Corado, J., F. 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