Abstract
Hepatitis C virus (HCV) replication was assessed before and during alpha‐interferon (IFN) treatment in 22 anti‐HCV positive patients with posttransfusion or sporadic chronic hepatitis (CH). Eleven patients were “responders” and 11 patients “non‐responders” to IFN. Thirteen anti‐HCV negative healthy subjects and five anti‐HCV negative patients with autoimmune CH served as controls.
Serum HCV‐RNA was detected by the polymerase chain reaction (PCR) in all untreated anti‐HCV positive patients but in none of the anti‐HCV negative subjects. PCR primers from the 5′‐non‐coding (NC) region were more sensitive than primers from a non‐structural (NS5) region in detecting HCV‐RNA (21/22, 95% vs. 7/22, 32%, respectively). Positive strand HCV‐RNA titre and positivity rate for the negative strand were similar in responders and non‐responders before IFN treatment, as well as anti‐cl00‐3 titre by enzyme‐linked immunosorbent assay (ELISA), and anti‐5‐1‐1, anti‐c33c, anti‐c22 positivity rate by immunoblot assay (RIBA). HCV‐RNA positivity by both NC and NS primers was more frequent before IFN among responders. During IFN treatment, serum HCV‐RNA was detectable, mostly at low titres, in 1 (NC positive) of the 11 responders and in 9 (4 NS positive and 5 NC positive) of the 11 non‐responders. Among the four non‐responders who were NS positive during IFN, three were NC positive before IFN.
Serum HCV‐RNA was always found in our post‐transfusion or sporadic anti‐HCV positive patients with CH. Viraemia generally decreased during IFN treatment, but no available HCV markers clearly distinguished responders from non‐responders before IFN treatment. Different NC and NS primers behaviour between responders and non‐responders before and during treatment with IFN suggests genomic heterogeneity and may explain non‐responsiveness to IFN. © 1992 Wiley‐Liss, Inc.