July 13, 2000
Thursday afternoon brought me to an oral session of papers on hepatitis C (HCV) and HIV co-infection (CoInf). We have seen a burgeoning interest and concern about hepatitis C in people with HIV infection. HCV progresses rapidly when associated with advanced HIV disease. We have only just recently begun systematic study of the interrelationships of these two infections. Very few studies have yet to be performed with treatment interventions for HCV in CoInf. I have seen reluctance on the part of physicians to prescribe therapy (i.e., interferon and ribavirin) for HCV until more data on the short- and long-term outcomes and adverse effects of these therapies are available.
Dr. Rockstroh, from Germany, described a cohort of hemophiliacs and IDUs with CoInf. CD4 was higher in the IDUs, but otherwise both groups were similar with respect to CD4, HIV viral load, HCV viral load, and liver function tests. The genotype strain of HCV can be correlated with either an improved or worsened prognosis (from liver disease). The hemophiliac co-infected patients tended to have both favorable and unfavorable genotypes; the IDUs tended to have unfavorable genotypes.
This study investigated the effect of HCV infection on HIV in CoInf patients. He looked at the EuroSIDA cohort PK over 8,500 HIV patients. Of these, 4,078 had HCV antibody testing; 33% were HCV-positive. Compared to those who were HCV-negative, the HCV-positive were more likely to be female, caucasian, younger, and less likely to have an AIDS diagnosis. During the follow-up period that averaged almost three years a higher percentage (16%) of those with CoInf died compared to those with HIV infection alone (12%). The risk of death was analyzed statistically and found to be associated with CoInf, increased age, lower CD4 counts and a baseline AIDS diagnosis.
A study that looked at combination therapy with IFN and RBV was presented during the this session by Landau from France. Sixty-six CoInf patients were treated with IFN (3 million units three times weekly) and oral RBV for six months in patients whose liver biopsies showed mild fibrosis and for 12 months in patients whose biopsies showed (or worse) fibrosis. All patients had pre-treatment liver biopsies. 57% of patients had genotype 1a or 1b, HCV viral loads were high, cirrhosis was common (42%). Overall only 24% of patients showed a sustained virologic response six months after completing therapy. The genotype 3a pts did better as expected, with 63% having a sustained response. Adverse effects were common leading to 23% discontinuing treatment and others reducing dosages of IFN or RBV or both.
Dr. Kravtchenko described the state of HCV/HIV coinfection in the Moscow region of Russia. He reported on an "exploding" epidemic of CoInf with approximately 90% of IDUs in that region having CoInf. The 3a genotype, which is generally associated with a favorable prognosis, occurred in 60%. Twenty-nine of their patients underwent liver biopsy revealing mild-moderate findings of fibrosis. He also reported on very preliminary data from a treatment trial using interferon and rimantidine (this is not the same as ribavirin).
Dr. Zaltron, et al., from Italy, discussed treatment of HCV in CoInf patients using interferon therapy alone (no ribavirin) or no therapy. In a group of 83 CoInf patients the early results, at the end of three months of therapy, were poor (only 34% suppressed HCV viremia) and not sustained after treatment was discontinued. The IFN treatment did not have serious adverse effects nor did it cause any significant change in CD4 counts or HIV viral load. We already know from studies in HCV-infected (without HIV) patients that IFN monotherapy does not work well, and does not work as well as combination therapy with ribavirin.