Distribution of Hepatitis C Virus Genotypes Determined by Line Probe Assay in Patients with Chronic Hepatitis C Seen at Tertiary Referral Centers in the United States

Lau, Johnson Y.N.; Davis, Gary L.; Prescott, L E; Maertens, Geert; Lindsay, Karen L.; Qian, Keping; Mizokami, Masashi; Simmonds, Peter

doi:10.7326/0003-4819-124-10-199605150-00002

Cited by 185 publications

(135 citation statements)

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“…Others have also found particularly low HCV RNA copy numbers in patients infected with HCV genotype 4. 58,59 Together with the current results, this suggests that HCV genotype 4 generally has lower RNA loads compared with genotypes 1-3. If this proves to be true, it could mean that future trials for HCV therapy in Egypt will be difficult to monitor using current techniques, given their sensitivity and/or their inability (with the exception of the bDNA assay) to quantify all HCV genotypes.…”

Section: Discussionsupporting

confidence: 82%

Hepatocellular carcinoma in Egyptians with and without a history of hepatitis B virus infection: association with hepatitis C virus (HCV) infection but not with (HCV) RNA level.

Yates

Hafez²,

Beld³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. The aim of this study was to analyze the association of hepatocellular carcinoma (HCC) with hepatitis C virus (HCV) in Egypt, using hepatitis B virus (HBV) and hepatitis E virus (HEV) as virus controls. In addition, the association of HCC with HCV RNA levels among persons seropositive for HCV was analyzed. We compared 131 patients with proven HCC, 247 with bladder cancer, and 466 healthy hospital employees. Age, sex, and place of residence were recorded to study confounding factors. Among the healthy controls, 16% were seropositive for HCV, 21% for HBV, and 31% for HEV. When healthy controls were age-matched with HCC patients, the latter were significantly (P Ͻ 0.001) more often HCV seropositive (67%) than were the controls (30%). The seropositivity for HBV and HEV did not differ significantly in frequency between the two groups. The seropositivity for HCV was also significantly (P Ͻ 0.001) more often found in HCC patients (76%) than in BC patients (47%), with seroprevalences for HBV and HEV not differing significantly in these age-matched groups. In HBV-negative HCC and bladder cancer patients, seroprevalence for HCV was significantly (P ϭ 0.002) higher in HCC patients (68%) than in bladder cancer patients (36%). This difference was even more pronounced (P Ͻ 0.001) in HBV-positive HCC and bladder cancer patients (78% versus 52%, respectively). Of HCV-seropositive individuals, 49% were HCV RNA positive by branched DNA assay, and of these, 96% were infected by HCV genotype 4. No correlation between HCV RNA load and seropositivity of HBV or age or disease state was found. Infection with HCV and HCV-HBV double infection, but not HBV or HEV infection alone, is strongly correlated with HCC in Egypt.Hepatitis C virus (HCV) causes more than 90% of parenterally transmitted non-A, non-B (NANBH) hepatitis.1-4 In more than 85% of HCV infections, the infection persists and leads to chronic hepatitis. 4,5 Once chronic hepatitis is established, it may slowly progress to worsening stages of fibrosis and cirrhosis and ultimately lead to the development of hepatocellular carcinoma (HCC). 1,[6][7][8] In the first two decades after acute HCV infection, both mortality and morbidity remain modest in frequency, but after this period both can be expected to increase.1,2 Infection with HCV is widely recognized as the most common indication for liver transplantation 9 in the United States, Europe, and Japan. Although no firm data are available, death rates for HCC in Egypt appear to be increasing over the last decade. 10,11 Hepatitis virus infections of any kind are highly prevalent in the general population. The relatively high prevalence of HCV infections in Egypt was first established in 1992 by Kamel and others. 12 Other groups thereafter found HCV seroprevalence rates ranging from 6% to 38% with an average of approximately 15%. [12][13][14][15][16] The reasons behind these high HCV infection rates being 5-35-fold higher than reported elsewhere in the world are still unknown. In Egypt, the HCV seroprevalence was 55% among ...

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Section: Discussionsupporting

confidence: 82%

Hepatocellular carcinoma in Egyptians with and without a history of hepatitis B virus infection: association with hepatitis C virus (HCV) infection but not with (HCV) RNA level.

Yates

Hafez²,

Beld³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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“…16,17 HCV genotype was determined by restriction fragment length polymorphism based at the 5Ј-untranslated genomic region. 18,19 The nomenclature of HCV genotypes was according to the system proposed by Simmonds et al 20 Liver Histology. Hematoxylin-eosin-stained liver sections from all patients were evaluated by two blinded, independent investigators for their portal, periportal, and lobular activity, as well as fibrosis, according to the criteria proposed by Knodell et al 21 Summation of the three activity scores (portal ϩ periportal ϩ lobular) constituted the histological inflammatory activity index, and summation of all scores reflected total Knodell score.…”

Section: Methodsmentioning

confidence: 99%

Intrahepatic hepatitis C virus-specific cytotoxic T lymphocyte activity and response to interferon alfa therapy in chronic hepatitis C

et al. 1998

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Hepatitis C virus (HCV)-specific cytotoxic T lymphocytes (CTL) have been shown to play a role in host defense and pathogenesis of chronic HCV infection. Our aim was to test the hypothesis that intrahepatic HCV-specific CTL activity may impact subsequent response to interferon alfa (IFN-␣) therapy. Of the 37 patients that we have prospectively evaluated for HCV-specific CTL activity in liver, 21 received IFN therapy, and 19 completed a 6-month course and attended 6 to 18 months of follow-up. Intrahepatic CD8 ؉ cells were isolated from liver biopsy tissue and tested against target cells expressing HCV antigens to determine intrahepatic CTL activity. The relationship between treatment response and HCV-specific CTL activity and other factors known to associate with response (genotype, viremia, histology) was analyzed. HCV-specific CTL activity was detected in 9 of 21 patients (and 9 of 19 who completed therapy). After 6 months of IFN therapy, 8 of 19 (42%) patients had normal serum alanine transaminase (ALT) (complete responders). After 18 months of follow-up, only 3 patients (16%) had a sustained biochemical response. Of the 9 patients with detectable HCV-specific CTL activity in their liver before treatment, 7 (78%) developed a complete response. In contrast, only 1 of the 10 patients with no detectable HCV-specific CTL activity developed a complete response to IFN (P F .01). In 6 of 8 patients with a complete response, including the 3 sustained responders, the CTL response appeared to be directed predominately to the HCV core region. These data suggest that the host immune response, particularly that mediated by CD8 ؉ CTL, may be important in determining the outcome of IFN therapy for chronic HCV infection. Further understanding of the mechanism of action of IFN should impact the design of better therapeutic strategies against chronic HCV infection. (HEPATOLOGY 1998;28:225-230.)The host cellular immune defense, including the CD4 ϩ and CD8 ϩ T-cell response, is activated in patients with hepatitis C virus (HCV) infection. The intensity of the T-cell response during the early stages of infection may be a critical determinant of disease resolution and control of infection. 1,2 In chronic viral infection, viral-specific CD8 ϩ cytotoxic T lymphocytes (CTL) have been shown to be important in host defense and in the control of the viral infection. [3][4][5][6][7] In lymphocytic choriomeningitis virus infection, virus-specific CTL activity reduces viral titers by 4 to 5 logs. 8 It is felt that CTL might lead to viral clearance through either direct lysis of infected cells or cytokine-mediated mechanisms. We and others have shown that HCV-specific CTL activity is detectable in the liver in a proportion of patients with chronic HCV infection. The presence of HCV-specific CTL activity in bulk-expanded CTL was found to be associated with a lower level of viremia and a greater inflammatory activity in the liver, suggesting that HCV-specific CTLs may assist in the control HCV infection, but, in so doing, contribute to hepatoce...

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“…1 The risk of progression of liver disease in these patients is influenced by both viral and host factors, [2][3][4][5] with histological features ranging from mild inflammation to severe fibrosis, as well as cancer. 6,7 Fibrosis develops as a multicellular process involving paracrine signaling between the resident liver cells and inflammatory cells.…”

Section: A Pproximately 4 Million People In the Unitedmentioning

confidence: 99%

Intrahepatic gene expression profiles and alpha‐smooth muscle actin patterns in hepatitis C virus induced fibrosis†

et al. 2005

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To gain insight into pathogenic mechanisms underlying fibrosis in hepatitis C virus (HCV)-mediated liver injury, we compared intrahepatic gene expression profiles in HCV-infected patients at different stages of fibrosis and ␣-smooth muscle actin (␣-SMA) staining patterns. We studied 21 liver biopsy specimens: 5 had no fibrosis (Ludwig-Batts stage 0); 10 had early portal or periportal fibrosis (stages 1 and 2); and 6, advanced fibrosis (stages 3 and 4). None of the patients had hepatocellular carcinoma. Transcriptional profiles were determined by high-density oligonucleotide microarrays. ANOVA identified 157 genes for which transcript abundance was associated with fibrosis stage. These defined three distinct hierarchical clusters of patients. Patients with predominantly stage 0 fibrosis had increased abundance of mRNAs linked to glycolipid metabolism. PDGF, a potent stellate cell mitogen, was also increased. Transcripts with increased abundance in stages 1 and 2 fibrosis were associated with oxidative stress, apoptosis, inflammation, proliferation, and matrix degradation, whereas transcripts increased in stages 3 and 4 were associated with fibrogenesis and cellular proliferation. Cells staining for ␣-SMA were detectable at all stages but infrequent in advanced fibrosis without active inflammation. A high frequency of such cells was associated with mRNAs linked to glycolipid metabolism. In conclusion, the presence of ␣-SMA-

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Distribution of Hepatitis C Virus Genotypes Determined by Line Probe Assay in Patients with Chronic Hepatitis C Seen at Tertiary Referral Centers in the United States

Cited by 185 publications

References 0 publications

Hepatocellular carcinoma in Egyptians with and without a history of hepatitis B virus infection: association with hepatitis C virus (HCV) infection but not with (HCV) RNA level.

Hepatocellular carcinoma in Egyptians with and without a history of hepatitis B virus infection: association with hepatitis C virus (HCV) infection but not with (HCV) RNA level.

Intrahepatic hepatitis C virus-specific cytotoxic T lymphocyte activity and response to interferon alfa therapy in chronic hepatitis C

Intrahepatic gene expression profiles and alpha‐smooth muscle actin patterns in hepatitis C virus induced fibrosis†

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