Estimating the Date of Hepatitis C Virus Infection from Patient Interviews and Antibody Tests on Stored Sera

Bruden, Dana; McMahon, Brian J.; Hennessy, Thomas W.; Christensen, Clayton M.; Homan, Chriss; Williams, James L.; Sullivan, Daniel G.; Gretch, David R.; Cagle, Henry H.; Bulkow, Lisa

doi:10.1111/j.1572-0241.2004.30826.x

Cited by 21 publications

(24 citation statements)

References 27 publications

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“…As in several previous reports, 6,9,24,31 fibrosis progression rate was calculated from a single liver biopsy and estimated disease duration. Potential inaccuracy in the presumed date of infection 32 was limited by exclusive enrollment of patients with a previous history of a single, well-identified route of exposure. The assumption of linearity of FPR has recently been disputed in a report suggesting late acceleration of fibrogenesis.…”

Section: Discussionmentioning

confidence: 99%

Daily Cannabis Smoking as a Risk Factor for Progression of Fibrosis in Chronic Hepatitis C *

Hézode¹,

Roudot‐Thoraval²,

Nguyen³

et al. 2005

Hepatology

259

191

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Cannabinoids present in Cannabis sativa (marijuana) exert biological effects via cannabinoid receptors CB1 and CB2. We recently demonstrated that CB1 and CB2 receptors regulate progression of experimental liver fibrosis. We therefore investigated the impact of cannabis smoking on fibrosis progression rate in patients with chronic hepatitis C (CHC). Two hundred seventy consecutive untreated patients with CHC of known duration undergoing liver biopsy were studied. Demographic, epidemiological, metabolic, and virological data were recorded, and detailed histories of cannabis, alcohol, and tobacco use over the span of hepatitis C virus infection were obtained.

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Section: Discussionmentioning

confidence: 99%

Daily Cannabis Smoking as a Risk Factor for Progression of Fibrosis in Chronic Hepatitis C *

Hézode¹,

Roudot‐Thoraval²,

Nguyen³

et al. 2005

Hepatology

259

191

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“…Certainly the use of FPRs in HCV disease models has inherent problems relating to liver biopsy staging and sampling errors, the assumption that liver injury follows a linear course, and inaccuracies in estimating the duration of infection. 31 The use of patient self-reporting for duration of infection may have led to a potential bias in our Kaplan-Meier baseline estimates for projected time to progression to cirrhosis, but this result would have affected the homozygous and heterozygous subgroups equally. Approximately half of the patients in this study had minimal fibrosis with slow FPRs that would make it difficult to detect any weak associations that may influence disease progression.…”

Section: Discussionmentioning

confidence: 98%

HLA class I allelic diversity and progression of fibrosis in patients with chronic hepatitis C

et al. 2006

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Patients infected with HIV-1 who are heterozygous at HLA class I loci present greater variety of antigenic peptides to CD8 ؉ cytotoxic T lymphocytes, slowing progression to AIDS. A similar broad immune response in chronic hepatitis C (CHC) infection could result in greater hepatic injury. Although specific HLA class II alleles may influence outcome in CHC patients, the role of HLA class I heterogeneity is generally less clearly defined. Our aims were to determine whether HLA class I allelic diversity is associated with disease severity and progression of fibrosis in CHC. The study population consisted of 670 adults with CHC, including 155 with advanced cirrhosis, and 237 non-HCV-infected controls. Serological testing for HLA class I antigens was performed via microlymphocytotoxicity assay. Peptide expression was defined as heterozygous (i.e., a different allele at each locus) or homozygous. The majority of these patients develop chronic infection, which is characterized by varying degrees of inflammation and hepatic fibrosis. A proportion of patients (Ͻ20%) will develop progressive liver damage with subsequent cirrhosis, end-stage liver disease, and hepatocellular carcinoma over 20 to 40 years. 3 The immunopathogenic mechanisms responsible for viral persistence and varying degrees of hepatic injury in chronic hepatitis C (CHC) are poorly understood. Cellular immune responses probably play an important role in this regard. CD4 ϩ T helper cells recognize HCV-derived peptides in the HLA class II binding groove of antigenpresenting cells such as dendritic cells, macrophages, and B cells. CD8 ϩ cytotoxic T cell lymphocytes (CTL) recognize intracellularly processed HCV proteins presented on HLA class I molecules on virus-infected cells. The HLA class I and II loci contain a highly polymorphic set of genes that appear to have evolved over time through selection pressures, thus allowing the host to resist a variety of pathogens. 4 In comparison with homozygous individuals, persons with overdominant selection or heterozygote advantage at HLA loci may be able to present a greater variety of antigenic peptides to T cells, thus result-

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“…Subjects classified as havn p 15 ing mild disease had either no (stage 0) or mild (stage 1) fibrosis in liver biospy samples obtained at an average interval of 0.1 years before study completion ( ). The estimated date of n p 33 HCV infection was assigned on the basis of the date of first injection drug use or blood transfusion exposure (before July 1992) and was correlated with seroconversion data generated from stored serum specimens, as described elsewhere [28]. Of 355 HCV genotype 1-infected patients in the cohort, 52 were selected for longitudinal study of viral dynamics on the basis of the number of historical serum specimens available for testing (minimum of 3 specimens spanning at least 5 years), completion of a current liver biopsy, and absence of laboratory or clinical evidence of hepatitis B virus or HIV coinfection.…”

Section: Subjects Materials and Methodsmentioning

confidence: 99%

Hepatitis C Virus Dynamics during Natural Infection Are Associated with Long‐Term Histological Outcome of Chronic Hepatitis C Disease

et al. 2007

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Estimating the Date of Hepatitis C Virus Infection from Patient Interviews and Antibody Tests on Stored Sera

Abstract: Inaccuracies in the length of HCV could occur in outcome studies that rely on patient recall of risk-factor history. Statistical methods that incorporate the uncertainty in assigning infection date are needed.

Cited by 21 publications

References 27 publications

Daily Cannabis Smoking as a Risk Factor for Progression of Fibrosis in Chronic Hepatitis C *

Daily Cannabis Smoking as a Risk Factor for Progression of Fibrosis in Chronic Hepatitis C *

HLA class I allelic diversity and progression of fibrosis in patients with chronic hepatitis C

Hepatitis C Virus Dynamics during Natural Infection Are Associated with Long‐Term Histological Outcome of Chronic Hepatitis C Disease

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