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To understand the effects of interferon treatment on immune system activation by chronic infections, we evaluated kinetic patterns of a broad spectrum of serum biomarkers during <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> treatment in <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> co\u2010infected patients. HCV viral load and 50 biomarkers were analysed at baseline and 27 time points during pegylated interferon\u2010alpha and ribavirin (<jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">RBV<\/jats:styled-content>) treatment of 12 <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> co\u2010infected patients. We evaluated biomarker changes from baseline for each time point and biomarker correlations with clinical parameters, treatment response and liver histopathology. IL\u20101<jats:italic>\u03b1<\/jats:italic>, IL\u201012p40, IL\u20101RA, IP\u201010, <jats:styled-content style=\"fixed-case\">MIG<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> MIP<\/jats:styled-content>\u20101<jats:italic>\u03b1<\/jats:italic>\/1<jats:italic>\u03b2<\/jats:italic>, HGF, <jats:styled-content style=\"fixed-case\">sCD<\/jats:styled-content>40L, <jats:styled-content style=\"fixed-case\">TRAIL<\/jats:styled-content> and leptin increased in the first day. IL\u201012p70, IL\u201017A, IL\u201010, GRO<jats:italic>\u03b1<\/jats:italic>, IL\u20108, MCP\u20103, IL\u20104 and M\u2010CSF peaked later during week 1. IL\u20101<jats:italic>\u03b1<\/jats:italic>, HGF, IP\u201010, MIP\u20101<jats:italic>\u03b1<\/jats:italic>, TRAIL, <jats:styled-content style=\"fixed-case\">sCD<\/jats:styled-content>40L, IL\u201010, IL\u201012p70, MCP\u20103, FGFb, ENA\u201078, TGF\u2010<jats:italic>\u03b2<\/jats:italic>, IL\u20102, IFN\u2010<jats:italic>\u03b3<\/jats:italic>, IL\u20106, IL\u201015, IL\u20107 and PDGF\u2010BB decreased below baseline over the course of treatment. Higher <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>, baseline <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> viral load and leptin levels were associated with lack of sustained virologic response. ENA\u201078 was associated with sustained viral response. Positive correlations were found between liver inflammation and baseline CD4 count, s<jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HGF<\/jats:styled-content>; fibrosis stage and <jats:styled-content style=\"fixed-case\">HGF<\/jats:styled-content>; liver steatosis, <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content> and leptin. Our findings suggest <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">RBV<\/jats:styled-content> treatment initially increases levels of several biomarkers, but eventually leads to a decline in many immune markers. These findings shed light on the relationship between <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content> treatment and immune activation by chronic viral infections, such as <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/jvh.12226","type":"journal-article","created":{"date-parts":[[2014,2,10]],"date-time":"2014-02-10T02:56:56Z","timestamp":1392001016000},"page":"25-36","source":"Crossref","is-referenced-by-count":10,"title":["Acute and chronic immune biomarker changes during interferon\/ribavirin treatment in <scp>HIV<\/scp>\/<scp>HCV<\/scp> co\u2010infected patients"],"prefix":"10.1111","volume":"22","author":[{"given":"M. K.","family":"Jain","sequence":"first","affiliation":[{"name":"Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B.","family":"Adams\u2010Huet","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences University of Texas Southwestern Medical Center Dallas TX USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Terekhova","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L. E.","family":"Kushner","sequence":"additional","affiliation":[{"name":"AIDS Research Center Veterans Affairs Palo Alto Health Care System Palo Alto CA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Bedimo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine University of Texas Southwestern Medical Center Dallas TX USA"},{"name":"Department of Internal Medicine North Texas VA Medical Center Dallas TX USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"X.","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences University of Texas Southwestern Medical Center Dallas TX USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Holodniy","sequence":"additional","affiliation":[{"name":"AIDS Research Center Veterans Affairs Palo Alto Health Care System Palo Alto CA USA"},{"name":"Department of Medicine Stanford University School of Medicine Stanford 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