Model-based estimates were broadly consistent with other sources of information on the HCV epidemic in Australia. These models suggest that the prevalence of HCV-related cirrhosis and the incidence of HCV-related liver failure and HCC will more than triple in Australia by 2020.

The risk of perinatal transmission of hepatitis C virus (HCV) from a cohort of 95 human immunodeficiency virus (HIV)-negative intravenous drug users (IVDU) is described, 89 of whom were positive for antibodies to HCV (anti-HCV). Infection, defined as the presence of HCV RNA in a serum sample collected from an infant at any time during follow-up, was detected in six of 63 (9.5%) infants born to HCV antibody-positive viraemic mothers. No mother who was HCV RNA negative at delivery transmitted HCV to her infant. Hepatitis C virus antibodies became undetectable in uninfected infants by 15 months, but persisted in all HCV-infected infants throughout follow-up. An abnormal alanine aminotransferase (ALT) level was observed on at least one occasion in all HCV-infected infants and in six occasions in uninfected infants. Two of the six HCV-infected infants became HCV RNA negative during follow-up by 27 and 29 months. Both of these infants had a large ALT elevation (mean peak ALT 398U l-1) at around 12 months of age. Analysis of a range of potential risk factors revealed that maternal HCV RNA load was important in predicting transmission, but suggested that other factors play a role in perinatal transmission from mother to child. No difference was found between mothers who transmitted HCV to their infants and those who did not for HCV genotype, duration of drug use, duration of methadone use, methadone dose, history of alcohol abuse, past hepatitis B virus (HBV) infection, mode of delivery, maternal and gestational age, birth weight and incidence of breast-feeding. Mothers who transmitted HCV to their infants had a longer duration between membrane rupture and delivery than the mothers who did not transmit (P = 0.03). HCV RNA was not detected in breast milk and colostrum samples from 38 viraemic mothers, including two who transmitted HCV to their infant.

Viral recurrence is universal after transplantation for hepatitis C infection. This may lead to difficulties in differentiating allograft dysfunction caused by chronic rejection from hepatitis C virus (HCV) recurrence. Cases of severe cholestatic hepatitis have also been reported in conjunction with reinfection of the graft with HCV. Patients receiving transplants for HCV-related liver disease were studied before and after transplantation by HCV RNA quantitation of serial serum samples. Four major clinical patterns of HCV recurrence could be distinguished posttransplantation: group 1, asymptomatic hepatitis with no significant symptoms; group 2, cholestatic hepatitis with centrilobular ballooning; group 3, hepatitis leading to chronic allograft rejection; and group 4, persistently normal serum aminotransferase levels. Pretransplantation viral load was shown to be an important indicator of disease severity because the group 2 patients had significantly higher pretransplantation viral loads than patients in group 1 (P ‫؍‬ 0.01) and group 4 (P ‫؍‬ 0.005). The group 2 patients also had persistently significantly higher posttransplantation viral loads than the patients in group 1 (P ‫؍‬ 0.01) and group 4 (P ‫؍‬ 0.02), whereas patients who developed chronic allograft rejection showed marked decreases in serum HCV RNA before retransplantation. Patients from group 4 had the lowest viral loads after transplantation. These results show that persisting graft cholestasis due to HCV is associated with persistently high HCV RNA levels compared with other etiologies of graft dysfunction. Prospective studies are needed to determine whether such quantitation may be diagnostically helpful in distinguishing the different patterns of HCV-related graft dysfunction observed after liver transplantation.

Recurrent hepatitis B virus (HBV)infection remains a major cause of morbidity and mortality after liver transplantation. Recently, antiviral therapy, such as lamivudine, has become available for prophylaxis against HBV reactivation posttransplantation and for the treatment of HBV recurrent disease. We report our initial experience with lamivudine therapy in patients with precore mutant-associated HBV infection undergoing liver transplantation (n ‫؍‬ 29). Outcomes were compared in three patient groups: group 1, precore mutant HBV infection not receiving lamivudine (n ‫؍‬ 10); group 2, recurrent precore mutant HBV infection posttransplantation subsequently treated with lamivudine (n ‫؍‬ 10); and group 3, HBV precore mutant patients undergoing liver transplantation and receiving lamivudine and low-dose hepatitis B immune globulin (HBIG) from the time of transplantation (n ‫؍‬ 9). In group 1, HBV recurred in 9 of 10 patients, with subsequent graft loss in all 9 patients. In group 2, all patients developed HBV recurrence at a mean of 7.3 months posttransplantation and started lamivudine therapy at a median of 16 months posttransplantation. Follow-up on lamivudine therapy was for a median of 11 months. Six of these 10 patients developed mutations in the HBV polymerase gene associated with lamivudine resistance. There were two liver failure-related deaths in this group. In group 3 patients, there was one death from graft-versus-host disease. The remaining 8 patients have been followed up for a mean of 15.6 months posttransplantation, and all remain hepatitis B surface antigen negative and HBV DNA negative. In conclusion, lamivudine therapy in association with low-dose HBIG is effective in preventing HBV reactivation posttransplantation. Rescue therapy with lamivudine in patients with HBV recurrence is only moderately effective, with a 60% lamivudine resistance rate in patients treated for longer than 6 months.

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