Specificity of anti-HCV ELISA assessed by reactivity to three immunodominant HCV regions

Mimms, Larry; Vallari, D S; Ducharme, Louise; Holland, Paul V.; Kuramoto, I. K.; Zeldis, Jerome B.

doi:10.1016/0140-6736(90)93377-2

Cited by 72 publications

(21 citation statements)

References 8 publications

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“…Antibodies to HCV gene products were assayed with a semiautomated dot blot immunoassay (MATRIX; Abbott Laboratories, North Chicago, IL) which employs an array ofpurified recombinant antigens spotted on nitrocellulose. This technology has been described in detail (17,18). The test panels consisted of the C-100 antigen, which was purchased from Chiron Corporation (Emeryville, CA), plus polypeptides corresponding to putative HCV NS-3 (33C), and 5'-structural sequences encoding for the putative core ofHCV (core) which were expressed in Escherichia coli as fusions with cytosine monophosphate keto deoxy octulosonate (CMP-KDO) synthetase (19).…”

Section: Methodsmentioning

confidence: 99%

Evidence for persistent hepatitis C virus (HCV) infection in hemophiliacs.

Allain¹,

Dailey²,

Laurian³

et al. 1991

J. Clin. Invest.

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Hepatitis C virus (HCV) is the major etiologic agent associated with non-A, non-B hepatitis. This study was designed to assess virologic and serologic markers in hemophiliacs exposed to non-heat-treated and/or virus-inactivated plasma derivatives. Serial bleeds from 48 hemophilic patients were analyzed for the presence of HCV viral RNA sequences as detected by polymerase chain reaction (PCR) and antibodies to structural (core) and nonstructural (C-100 and 33C) proteins by specific dot immunoblot assay. All patients exposed to non-heat-treated products, and four of six patients exposed only to virus inactivated products, had evidence of HCV infection. However, over the 5-yr study period, six exposed patients (13%) consistently lacked detectable anti-C-100 and seven (15%) lost this antibody. HCV viremia (PCR positive) was found in 91% of exposed patients, and was significantly more frequent in HIV seropositive hemophiliacs (P < 0.05). Six patients had high antibody level to HCV and elevated ALT, but appeared to clear viremia. Four hemophiliacs were HCV seropositive but lacked detectable viremia. These data indicate that hemophiliacs remain persistently infected by HCV and that antibody to the core antigen of HCV is a reliable marker of this transfusion transmissible agent. (J. Clin. Invest. 1991. 88:1672-1679

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Section: Methodsmentioning

confidence: 99%

Evidence for persistent hepatitis C virus (HCV) infection in hemophiliacs.

Allain¹,

Dailey²,

Laurian³

et al. 1991

J. Clin. Invest.

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“…The second-generation anti-HCV assays incorporated recombinant proteins originating from the core, NS3, and NS4 protein [Mimms et al, 1990;Bresters et al, 1992]. Regions within NS3 and core are more immunogenic and are more highly conserved than the NS4 region allowing improved detection of antibodies in individuals infected with all HCV genotypes.…”

Section: Introductionmentioning

confidence: 99%

Genotype dependence of peptide‐based immunoassays for the detection of HCV core antibodies

Muerhoff

Gutierrez

Kyrk

et al. 2008

Journal of Medical Virology

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Detection of hepatitis C virus (HCV) antibodies is partially influenced by the genotype of the infecting isolate. Immunoassays using genotype-1a-derived recombinants or peptides results in diminished reactivity among individuals infected with heterologous genotypes. We examined the magnitude of this effect on detection of core antibodies by using genotype-1a-derived core peptide immunoassays to test 254 HCV anti-core-positive individuals infected with genotypes 1-4 or 6. Peptides corresponding to amino acids 1-18, 10-24, and 11-28 reacted with 60%, 89%, and 85% of all samples, respectively. Peptide 1-18 detected 78% of individuals infected with genotype-1 or 2 but only 43% of those infected with genotypes 3, 4, or 6. Genotype-dependent reactivity was also observed for peptides 10-24 and 11-28. The use of a 34-mer peptide (encompassing amino acids 10-43) within the immunodominant region detected antibodies in 100% of specimens, thereby eliminating the genotype-dependent antibody detection observed with shorter peptides. Sequence differences between peptides and core of the infecting isolate did not entirely account for the genotype-dependent reactivity since some individuals displayed reactivity to peptides containing up to seven amino acid differences relative to the sequence of the infecting isolate, while others with identical core sequences had little or no reactivity. Thus, HCV core sequence divergence accounts for only a portion of the differential core antibody detectability observed when non-type-specific peptides are used. Differences in immune response between individuals infected with identical isolates also plays a significant role in core antibody detection using short peptides.

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“…Table 1 shows the laboratory data on the second admission. The antibody against HCV (HCVAb) was detected by the second generation enzyme-linked immunosorbent assay (ELISA) (2). Ultrasonography of the abdomen showed splenomegaly ( 147 x 48 mm)and a high echoic mass in the 5th and 8th segments of the liver.…”

Section: Case Reportmentioning

confidence: 99%

Sequential Occurrence of Hepatocellular Carcinoma Following Waldenstroem's Macroglobulinemia: The Pathogenetic Role of Chronic Liver Disease.

Izumi

Sasaki²,

Tsunoda³

et al. 1996

Intern. Med.

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Wereport a case of sequential occurrence of hepatocellular carcinoma (HCC)following Waldenstrom's macroglobulinemia (WM)in the course of chronic liver disease. The diagnosis of WM was madein a 55-year-old manwith a history of alcohol abuse. He developed HCCin the course ofWM,and hepatitis C virus (HCV) infection was detected by enzyme-linked immunosorbent assay. Recent reports suggest that persistent HCVinfection is related to the pathogenesis ofB cell malignancy. Chronic liver disease may be associated with the pathogenesis of the double malignancies in the present case. (Internal Medicine 35: 416-418, 1996)

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Specificity of anti-HCV ELISA assessed by reactivity to three immunodominant HCV regions

Cited by 72 publications

References 8 publications

Evidence for persistent hepatitis C virus (HCV) infection in hemophiliacs.

Evidence for persistent hepatitis C virus (HCV) infection in hemophiliacs.

Genotype dependence of peptide‐based immunoassays for the detection of HCV core antibodies

Sequential Occurrence of Hepatocellular Carcinoma Following Waldenstroem's Macroglobulinemia: The Pathogenetic Role of Chronic Liver Disease.

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