Hepatitis C virus transmission, 1988-1991, via blood components from donors subsequently found to be anti-HCV-positive

The recipients of blood components, from the first 12 anti-hepatitis C virus (HCV) positive donors identified by blood donor screening, 1985-1991, were traced retrospectively and tested to assess the HCV transmission rate, HCV genotypes and disease severity. Three enzyme-linked immunosorbent assay (ELISA) positive but RIBA-indeterminate and HCV RNA-negative donors did not transmit HCV to their 9 traced recipients. Nine RIBA- and HCV RNA-positive donors had donated blood to 27 now living recipients of whom 16/27 (59%) were viraemic 1-5 years later. Nine recipients had resolved infection, as determined by PCR HCV RNA. Five of these were RIBA-2 positive but HCV RNA-negative and 4 recipients were RIBA-2-indeterminate and HCV RNA-negative. Two recipients negative in all tests had probably received blood before the donor became infected with HCV. The HCV genotype in each case was identical between the donor and the recipient. Of the viraemic recipients, 50% (8/16) were unsuitable for further investigation or therapy due to their high age and/or underlying severe disease. At most, only 30% (8/27) of the recipients were suitable for further investigation and/or treatment. Two of these were already diagnosed as being infected with HCV before being traced. It is concluded that the benefit of a general tracing of recipients of blood components from HCV-infected donors is doubtful since only a few of them are suitable candidates for treatment. Our results seem to indicate that it is more appropriate to recommend anti-HCV testing to those seeking medical care who have received transfusions or undergone major surgery before 1992, i.e. before anti-HCV-screening was initiated

Health-related quality of life in patients with different stages of liver disease induced by hepatitis C

Objective. Patients with hepatitis C have been shown to have impaired health-related quality of life (HRQoL). The aim of this study was to determine HRQoL in patients in different stages of hepatitis C virus (HCV) and to compare HRQoL in HCV cirrhosis with non-HCV-induced cirrhosis. Material and methods. Out of 489 consecutive patients who fulfilled the inclusion criteria, 472 (96%) agreed to participate in the study: 158 patients with mild/moderate fibrosis with chronic hepatitis C (CHC group), 76 patients with HCV compensated cirrhosis (CC), 53 patients with HCV decompensated (DC) cirrhosis, 52 non-cirrhotic patients with sustained viral response (SVR), and a control group consisting of 32 patients with non-HCV CC and 101 with non-HCV DC who completed the Short Form-36 (SF-36) and EQ-5D questionnaire. Results. The CHC group had significantly lower SF-36 scores than healthy controls, with the exception of scores for the dimensions physical function and bodily pain. HCV patients with DC had lower scores in all SF-36 dimensions in comparison with those of the CHC group, as well as in physical and mental component summaries (P<0.001). In comparison with the CHC group, the HCV CC group had lower scores on the SF-36 general health dimension (p <0.05) and lower SF-36 physical component summary (PCS) scores (p <0.05). No major differences were seen in patients with HCV- and non-HCV-induced cirrhosis. Conclusions. Impairment in HRQoL in patients with HCV was associated with the severity of liver disease, patients with decompensated cirrhosis exhibiting the highest impairment in HRQoL. The etiology of liver disease does not seem to be important in determining HRQoL in cirrhosis

Genotyping of hepatitis C virus isolates by a modified polymerase chain reaction assay using type specific primers: epidemiological applications

A polymerase chain reaction (PCR)-based assay using primers against the hepatitis C core gene has been described [Okamoto et al. (1992a): Journal of General Virology 73:673-679]. Within the two major HCV genotypes 1 and 2, the Okamoto system identifies two subtypes each (1a, 1b and 2a, 2b, respectively). Typing is achieved by a primary PCR with consensus primers followed by a nested PCR with type specific primers. The original assay was modified by addition of a parallel second PCR identifying the recently described major genotype 3. The assay also identifies in duplicate subtype 1b (type II by Okamoto), suggested to respond poorly to interferon. Reaction conditions were reviewed and melting temperatures of all typing primers equalised to increase strigency. The modified system functioned well and typing results were supported by partial core sequencing. The following distribution of genotypes was found in 53 hepatitis C virus (HCV) infected Swedish blood donors: genotype 1a (57%), 3 (19%), 1b (13%), and 2b (11%). In six recipients of HCV infected blood identified in a retrospective study, the recipient HCV genotype was identical to donor HCV genotype. Furthermore, in HCV positive couples identical genotype was observed when only one partner had an external risk factor; whereas genotypes were often diverse if both sex partners had parenteral risk factors. Finally, a cluster of hepatitis C cases in a haemodialysis unit was evaluated retrospectively. Eight patients had genotype 1b, two had mixed 1a and 1b, and one had type 1a. The modified HCV genotyping assay was of value in examining different epidemiological situations and can be expanded presumably to include future genotypes