Influence of viraemia and genotype upon serological reactivity in screening assays for antibody to hepatitis C virus

Dhaliwal, S.K.; Prescott, L E; Dow, B. C.; Davidson, Fiona; Brown, Helen; Yap, P. L.; Follett, E. A. C.; Simmonds, Peter

doi:10.1002/(sici)1096-9071(199602)48:2<184::aid-jmv11>3.3.co;2-b

Cited by 6 publications

(6 citation statements)

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“…As diagnostic tests for the detection of HCV antibodies are based on recombinant antigens of HCV genotype 1, there has been speculation that such screening assays may lack sensitivity for detection of non‐genotype 1 infections. Consistent with this, a reduced reactivity to HCV genotype 2 and 3 has been reported in the third generation antibody screening assays 10 . In addition to virus variation influencing detection, infections may not be detected because of an inadequate serological response in patients who are immunocompromised or immunosuppressed.…”

Section: Introductionsupporting

confidence: 59%

New hepatitis viruses: Contenders and pretenders

Bowden

2001

J of Gastro and Hepatol

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Following the development of tests for hepatitis C virus and hepatitis E virus infection, it became clear that there remained cases of hepatitis that were non‐A‐E. Such cases provided impetus for the search for additional hepatitis viruses and, by using molecular techniques, several candidates were identified. An enteric agent responsible for sporadic non‐A and non‐E hepatitis was tentatively called hepatitis F virus. However, the lack of any corroborating reports has cast doubt on its status as a true hepatitis virus. Two groups independently reported the isolation of a blood‐borne virus, designated as hepatitis G virus (HGV) and GB virus C (GBV‐C) by their respective discoverers. They were later shown to be isolates of the same virus. While the virus has a high prevalence in cases of non‐A‐E hepatitis, it also has a high prevalence in the appropriate control groups and convincing evidence for its replication in the liver is lacking. Another possible hepatitis virus, TT virus, was discovered in the blood of a patient with post‐transfusion non‐A‐E hepatitis. By using PCR primers designed to overcome the high nucleotide sequence divergence, TT virus was found to be ubiquitous with a worldwide distribution. A disease association is thus unlikely. Most recently, a DNA virus designated as SEN‐V has been announced as a major cause of non‐A‐E hepatitis. Based on limited data available to researchers, SEN‐V is the most convincing contender for the new hepatitis virus title. However, the lessons learnt from the hepatitis virus pretenders will need to be applied to SEN‐V and any future contenders.

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Section: Introductionsupporting

confidence: 59%

New hepatitis viruses: Contenders and pretenders

Bowden

2001

J of Gastro and Hepatol

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“…4b) in this study confirmed the data reported by Nikolaeva et al (2002), who showed a range of 1 : 800-1 : 40 000 of anti-core IgG titres in chronic HCV and an antibody titre value of 1 : 5-1 : 200 in a recovered group. Because of the lack of variation of high anti-HCV reactivity in donors chronically infected with different genotypes using the HCV 3.0 ELISA, it was unlikely that a reliable correlation between anti-F and anti-HCV could be found in terms of the S : CO ratio, even though a 4-4.5-fold greater seroreactivity of genotype 1 samples compared with genotype 2 or 3 was reported using a commercial assay (Dhaliwal et al, 1996). However, the higher correlation between anti-F and anti-core antibody levels in genotypes 1 and 2 than in genotype 3 suggest that the F protein produced along with core protein during natural HCV infection is cross-reactive but potentially genotype-specific.…”

Section: Discussionmentioning

confidence: 99%

Differential reactivity of putative genotype 2 hepatitis C virus F protein between chronic and recovered infections

Chuang

Allain

2008

Journal of General Virology

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To date, all studies regarding hepatitis C virus (HCV) F protein have been based on expression in vitro/in vivo of recombinant protein or monoclonal antibodies derived from genotype 1a or 1b sequences, but not from other genotypes. The objective of this study was to prepare a putative genotype 2 recombinant F protein and evaluate its reactivity in plasma from individuals with chronic HCV infection or who had recovered from infection. One genotype 2 strain was selected for F protein (F-2) and core expression in bacterial culture. An ELISA was developed and applied to samples from patients with chronic infection or recovered infection of various genotypes. The anti-F-2 response in 117 samples showed a significantly higher reactivity in chronic than in recovered HCV-infected blood donors (P<0.001), but no difference was found among genotypes. However, the correlation between anti-F and anti-core was more significant in genotypes 1 and 2 than in genotype 3. Anti-F-2 titres were also significantly higher in chronic than in recovered individuals (P<0.0001). Antibody titres to recombinant genotype 2 core protein or to genotype 1 multiple proteins used in commercial anti-HCV assays paralleled the anti-F-2 end-point antibody titre. This study thus demonstrated the antigenicity of genotype 2 HCV F protein, although the exact location of the natural frameshift position remains unknown. The difference in anti-F-2 response between chronic and recovered infection, the cross-reactivity irrespective of genotype and the correlation of antibody response with structural and non-structural antigens suggest that the immune response to F protein is an integral part of the natural HCV infection.

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“…To achieve a more reliable diagnosis, sera with positive results in an EIA should always be retested by a confirmatory assay based on immunodominant antigens clearly different from those used in screening assays to exclude both assays from detecting the same false reactivity (11). Second, HCV diagnosis is hampered by the restriction of antigens used in commercially available tests to genotype 1a, which is predominantly found in the United States; these antigens do not necessarily represent viral genotypes found in other parts of the world (3,5,8). Thus, our confirmatory assay based on local isolates proved to be superior to commercial assays (6) and led to a very low number of patients for whom a final diagnosis was not possible (1.7%).…”

mentioning

confidence: 99%