{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T20:23:51Z","timestamp":1787862231747,"version":"build-2784847793"},"reference-count":44,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,3,8]],"date-time":"2016-03-08T00:00:00Z","timestamp":1457395200000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["HLA"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Chronic hepatitis B virus (<jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>) infection occurs in association to a deregulation of immune system. Human leukocyte antigen E (<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E) is an immune\u2010tolerant nonclassical <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content> class I molecule that could be involved in <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> progression. To measure soluble (s) <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E in patients with chronic <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> hepatitis (<jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content>). We tested the potential association of <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E*01:01\/01:03<\/jats:italic> A &gt; G gene polymorphism to <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content>. Our cohort consisted of 93 Tunisian <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients (stratified in <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> with high <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> levels and <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> with low <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> levels) and 245 healthy donors. Plasma <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E was determined using enzyme\u2010linked immunosorbent assay (<jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>). Genotyping was performed using polymerase chain reaction sequence\u2010specific primer. No association between <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E*01:01\/01:03<\/jats:italic> A &gt; G polymorphism and <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> levels in <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients was found. G\/G genotype is less frequent in <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients without significance. <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E is significantly enhanced in <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients compared with healthy controls (<jats:italic>P<\/jats:italic> = 0.0017). Stratification according to <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> levels showed that <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients with low <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> levels have higher <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E levels compared with <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients with high <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> levels. <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients with G\/G genotype have enhanced <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E levels compared with other genotypes (<jats:italic>P<\/jats:italic> = 0.037). This significant difference is maintained only for <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> women concerning G\/G genotypes (<jats:italic>P<\/jats:italic> = 0.042). Finally, we reported enhanced <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E in <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> patients with advanced stages of fibrosis (<jats:italic>P<\/jats:italic> = 0.032). We demonstrate, for the first time, the association of <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E to <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content>. Owing to the positive correlation of <jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E*01:01\/01:03<\/jats:italic> A &gt; G polymorphism and the association of <jats:styled-content style=\"fixed-case\">sHLA<\/jats:styled-content>\u2010E to advanced fibrosis stages, <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E could be a powerful predictor for <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> progression. Further investigations will be required to substantiate <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010E role as a putative clinical biomarker of <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/tan.12767","type":"journal-article","created":{"date-parts":[[2016,3,9]],"date-time":"2016-03-09T03:48:01Z","timestamp":1457495281000},"page":"153-159","source":"Crossref","is-referenced-by-count":19,"title":["<scp>HLA<\/scp>\u2010E polymorphism and soluble <scp>HLA<\/scp>\u2010E plasma levels in chronic hepatitis B patients"],"prefix":"10.1111","volume":"87","author":[{"given":"I.","family":"Zidi","sequence":"first","affiliation":[{"name":"Laboratory Microorganismes et Biomol\u00e9cules Actives, Sciences Faculty of Tunis University of Tunis El Manar  Tunis Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. B.","family":"Laaribi","sequence":"additional","affiliation":[{"name":"Laboratory Microorganismes et Biomol\u00e9cules Actives, Sciences Faculty of Tunis University of Tunis El Manar  Tunis Tunisia"},{"name":"Laboratory of Microbiology and Immunology, UR12SP34 University Hospital Farhat Hached  Sousse Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Bortolotti","sequence":"additional","affiliation":[{"name":"Department of Experimental and Diagnostic Medicine, Section Microbiology University of Ferrara  Ferrara Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Belhadj","sequence":"additional","affiliation":[{"name":"Laboratory of Microbiology and Immunology, UR12SP34 University Hospital Farhat Hached  Sousse Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Mehri","sequence":"additional","affiliation":[{"name":"Laboratory of Microbiology and Immunology, UR12SP34 University Hospital Farhat Hached  Sousse Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. B.","family":"Yahia","sequence":"additional","affiliation":[{"name":"Laboratory Microorganismes et Biomol\u00e9cules Actives, Sciences Faculty of Tunis University of Tunis El Manar  Tunis Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W.","family":"Babay","sequence":"additional","affiliation":[{"name":"Laboratory Microorganismes et Biomol\u00e9cules Actives, Sciences Faculty of Tunis University of Tunis El Manar  Tunis Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Chaouch","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Infectious Diseases University Hospital Farhat Hached  Sousse Tunisia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Zidi","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Ibn Al Jazzar University of Sousse  Sousse 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