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Increased levels of serum amyloid A during the early phase of hepatitis C treatment with interferon are associated with sustained virologic response - a pilot study.

Clearance of hepatitis C virus (HCV) infection has been associated with a strong, broadly-targeted T cell response [1, 2]. Activation of T-cells by HCV proteins results in production of soluble cytokines, which in turn induce various acute-phase proteins including serum amyloid A (SAA). It has been shown that SAA inhibits replication of HCV in vitro by blocking virus entry into the hepatocytes [3]. We therefore hypothesized that SAA levels measured during the early phases of HCV-therapy might predict the success of antiviral treatment. We studied 35 consecutive patients with chronic hepatitis C (males/females: 20/15; mean age±SD: 42.0±8.5, range: 23-61 years), who had been treated with peginterferon (pegIFN) plus ribavirin at our centre. HCV genotype (GT)-1 was most prevalent (n=17), followed by GT-3 (n=9), GT-4 (n=7), and GT-2 (n=1); one patient was coinfected with GT-1 and GT-4. All patients received pegIFN α -2a 180μg once weekly plus ribavirin (1000-1200mg daily for GT-1/4 and 800mg daily for GT-2/3). In patients with GT-1 or 4, treatment duration ranged from 24 to 72 weeks and was adapted to the kinetics of HCV-RNA during therapy as described previously [4]. In patients with GT-2 or 3, treatment duration was 24 weeks. Plasma HCV-RNA levels were measured by COBAS TaqMan HCV-RNA assay, version 2.0 (Roche). Plasma samples that were collected at