One of 87 healthy individuals with normal alanine aminotransferase activity was positive for antibody against only the viral core, but was negative for HCV RNA.
During treatment, the levels of alanine aminotransferase showed a significant decrease in all patients and the amount of HCV RNA fell from 1 fg/ml, 1 pg/ml, and greater than 10 pg/ml to 0.1 fg/ml, 100 fg/ml, and 1 pg/ml, respectively.
The influence of viremia on hepatic injury in patients infected with hepatitis C virus was examined by analysis of the relationship between alanine aminotransferase activity and the amount of hepatitis C virus RNA in sequential serum samples from I untreated patient with acute hepatitis C and 3 untreated patients with chronic hepatitis C. Semiquantitative analysis by the competitive-reverse-transcription/polymerase-chain-reaction method indicated that the quantity of hepatitis C virus RNA in the serum affected the disease activities of acute and chronic hepatitis C through their natural clinical courses in all these patients.
Of the 15 well-defined cases of PT-NANBH that showed multiple ALT peaks and hepatitis C virus seroconversions, 11 (73.3%) were shown to be transfused with at least one unit of blood positive for the antibody.
As a prelude to the development of nucleic acid probes specific for non-A, non-B hepatitis virus(es) (NANBV), plasmas with alanine aminotransferase levels greater than or equal to 110 IU were assayed for DNA by a radioimmunoassay.
In all cases, plasma HCV-RNA disappeared with the improvement of the initial alanine aminotransferase (ALT) elevation, but HCV-RNA reappeared about 1 year later with or without deterioration of the hepatitis.
Similarly, in five cases in previously infected recipients, defined as re-infection, 4/5 showed clinical hepatitis, the time to elevation of ALT was 30-46 days (34.8 +/- 6.4), and 5/5 and 3/5 were persistently positive for anti-HCV and HCV-RNA, respectively, for more than 1 year.
Thus hepatitis C virus replicates continually in a majority of patients with chronic hepatitis C, although some cases may show intermittent replication, and replication of hepatitis C virus does not always correlate with elevated ALT.
A complete response was defined as continuous normalization of the serum alanine aminotransferase (ALT) level and continuous disappearance of serum hepatitis C virus RNA (HCV-RNA) during interferon administration and more than 6 months after.
Among HCV RNA-positive subjects, mean age (p < 0.05), mean ALT (p < 0.001), signal-to-cutoff (S:CO) ratio on second-generation enzyme-linked immunosorbent assay (p < 0.001), and gamma globulin levels (p < 0.05) were higher than those among HCV RNA-negative subjects.
Of 83 spouses, 14 (16.9%) had elevated serum aspartate aminotransferase or alanine aminotransferase, 20 (24.1%) had detectable anti-HCV antibodies, and 17 (20.5%) had measurable HCV-RNA in serum.
However, there was no difference in alanine transaminase (ALT) levels, histological lesions, and RIBA-2 patterns in blood donors infected with either HCV genotype I or HCV genotype II.
All responders, defined as those individuals with normal alanine transaminase (ALT) levels at 48 weeks after therapy, had less than 2 x 10(6) HCV RNA Eq/mL before administration of IFN.
HCV RNA was detectable in 75% of the donors with elevated (> 45 U/L) alanine transaminase (ALT) values and in 59% of those with normal ALT levels (P = not significant).
The outcome of treatment was not correlated with race, age, sex, histology, and pretreatment ALT level, but was significantly (P < 0.00001) associated with the presence of both the NS4-JK-1 region and HCV type II.