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1.  Community acquired viral hepatitis B and C in the United States. 
Gut  1993;34(2 Suppl):S17-S19.
In the United States, most reported cases of hepatitis B occur in adults as a result of behavioural, lifestyle, or occupational exposures, but a significant number of children also become infected in well defined settings. Although only 1-3% of acute hepatitis B virus (HBV) infections occur in children under 5 years of age, they account for 20-30% of all chronic infections. A new strategy for HBV prevention in the USA includes integration of HBV vaccine into childhood immunisation schedules. Vaccination strategies that target high risk groups have not been effective. To determine the frequency and severity of community acquired chronic hepatitis C, patients with acute non-A, non-B hepatitis identified in four sentinel counties in the United States were followed prospectively. Hepatitis C virus (HCV) infection was found in 106 (82%) of 130 patients. Ninety three per cent of the HCV positive patients had a risk factor for their infection: 59% parenteral, 6% sexual or household, and 28% low socioeconomic level. Chronic hepatitis developed in 62%, independently of the risk factor for infection. HCV-RNA persisted in most patients, including those with biochemical resolution of their hepatitis. This study suggests that HCV may be a major cause of liver disease and persistent viraemia in the United States.
PMCID: PMC1373998  PMID: 8314488
2.  Sequence variation within a nonstructural region of the hepatitis G virus genome. 
Journal of Virology  1997;71(9):6875-6880.
Nine sets of nested PCR primers from a 2.6-kb region of the hepatitis G virus (HGV) genome at nucleotide positions 5829 to 8421 were designed and used to analyze serum specimens obtained from patients with community-acquired non-A, non-B hepatitis who were HGV RNA positive. One set of primers was found to be most efficient in detecting HGV and was subsequently used to test 162 HCV-positive and 11 HCV-negative plasma units obtained from individual paid donors. HGV RNA was detected in 30 (17.3%) plasma units, 2 of which were found among the 11 HCV-negative specimens. A complete set of nine PCR fragments was obtained from two patients with community-acquired acute non-A, non-B hepatitis and from four paid donors. All PCR fragments were sequenced and were shown to have a nucleotide similarity of 85.9 to 92.3% and a derived amino acid similarity of 96.0 to 99.0%. The majority of nucleotide changes occurred in the third position of codons. The HGV nucleotide and protein sequences obtained in this study were compared with HCV sequences. Based on this analysis the 2.6-kb fragment was predicted to encode the C-terminal part of the putative NS4b, the entire NS5a, and almost the complete NS5b proteins. Putative protease cleavage sites separating these proteins were also predicted. In serial specimens obtained from the two HGV-infected patients, no significant variations were found in the HGV nucleotide and derived amino acid sequences over time. The HGV sequences obtained from one patient showed no changes over 6 months, whereas more than 99.0% homology was observed for sequences from the second patient over 2.5 years. Heterogeneity analysis performed on 10 sequences obtained in this study and corresponding regions from 6 known full-size sequences of the HGV genomes demonstrated notable discrete heterogeneity consistent with the existence of HGV genetic groups or types.
PMCID: PMC191969  PMID: 9261413
3.  Hepatitis B virus precore mutation and fulminant hepatitis in the United States. A polymerase chain reaction-based assay for the detection of specific mutation. 
Journal of Clinical Investigation  1994;93(2):550-555.
Hepatitis B virus (HBV) variants with precore mutation(s) resulting in the absence of HBeAg production have been associated with the occurrence of fulminant hepatitis in Japan, Israel, and southern Europe, where the prevalence of this HBV strain appears common. In areas such as United States, where HBV infection is not endemic, the role of this mutant virus in fulminant hepatitis is unknown. We developed an amplification refractory mutation detection system to detect specifically the presence of the G to A mutation at nucleotide position 1898, which is the most frequently observed mutation resulting in a precore stop codon. In addition, this method provided a quantitative measurement of the relative ratio of one strain to the other. Using this system, we tested HBV strains for the presence of the stop codon mutation in sera from 40 cases of fulminant hepatitis B occurring in the United States. Serum HBV DNAs from 28 patients were analyzed successfully. A mixture of wild-type and mutant strains in various ratios were observed in 15 patients, wild type exclusively in 11, and mutant exclusively in 2. Four of these patients had undergone liver transplantation for HBV-associated cirrhosis and developed fulminant HBV-associated hepatitis after transplantation. Pre- and posttransplant serum samples from one patient were analyzed: a mixture of wild-type and mutant HBV strains was detected in both samples. Our study demonstrated that both wild-type and mutant HBV strains are associated with fulminant hepatitis, and that in some patients in the United States, factors other than precore mutations contribute to the development of fulminant hepatitis.
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PMCID: PMC293877  PMID: 8113393

Results 1-3 (3)