Serological diagnosis of acute viral hepatitis

Hoofnagle, Jay H.; Ponzetto, Antonio; Mathiesen, Lars; Waggoner, Jeanne G.; Bales, Z B; Seeff, Leonard B.

doi:10.1007/bf01315598

Cited by 39 publications

(26 citation statements)

References 28 publications

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“…These assays use either monoclonal or polyclonal anti-HBs bound to a solid phase and a second labeled anti-HBs to detect the captured antigen. Despite the high performance of screening assays, transfusion-associated HBV infection is still reported (13,14,18). There are three possibilities to explain false-negative results in commercial assays.…”

mentioning

confidence: 99%

Evaluation of Two New Automated Assays for Hepatitis B Virus Surface Antigen (HBsAg) Detection: IMMULITE HBsAg and IMMULITE 2000 HBsAg

et al. 2003

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The envelope protein of hepatitis B virus (HBV), HBV surface antigen (HBsAg), is a transmembrane glycoprotein usually shed in large amounts in the serum of infected individuals, where it is found as spherical particles with a diameter of 22 nm or filaments of similar diameter (29). The a determinant of HBsAg, a predicted double-loop structure projecting from the surface of the HBV particle (28), is the major neutralizing epitope. Antibodies to the a determinant confer protection in adults to all the common subtypes of HBV. Within the predicted loop regions are also located subtype determinants d or y and w or r. A total of nine serotypes have been described (9). These have been related to six genomic groups, groups A to F based, on sequencing of the S gene of isolates from different geographical regions (23,24).HBsAg is one of the first serum markers to appear during the course of HBV infection and can be detected 2 to 8 weeks before biochemical evidence of liver dysfunction and the onset of jaundice. HBsAg is cleared within a few months in selflimiting illness. If HBsAg persists for more than 6 months, spontaneous clearance is very unlikely and the infected individual is considered to be a chronic HBV carrier.Among the many commercially licensed HBsAg assays offered, enzyme-linked immunosorbent assays are the most commonly used. These assays use either monoclonal or polyclonal anti-HBs bound to a solid phase and a second labeled anti-HBs to detect the captured antigen. Despite the high performance of screening assays, transfusion-associated HBV infection is still reported (13,14,18). There are three possibilities to explain false-negative results in commercial assays. In chronic HBV carriers, the HBsAg level may be below the detection limit; i.e., a high proportion of individuals with antibodies against HBV core antigen (anti-HBc) as the only serological marker of infection are low-level chronic carriers of the virus (12, 17). Another explanation is that virus variants yield sequences that are not recognized by the antibodies employed in the assays. In different geographical locations, vaccine-escape mutants are emerging under the selective pressure of active immunization, and there is a danger that they will become dominant strains as vaccination becomes universal (5, 15). Breakthrough infections due to point mutations of the a determinant have been described in Europe, Africa, and Asia (4,6,11,25,26,30). Vaccine-escape mutants within the a determinant of the S gene are not as effectively recognized by conventional diagnostic tests as wild-type particle (7,16). A further explanation is that there are variants in other parts of the genome that down-regulate the production of HBsAg (3).

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confidence: 99%

Evaluation of Two New Automated Assays for Hepatitis B Virus Surface Antigen (HBsAg) Detection: IMMULITE HBsAg and IMMULITE 2000 HBsAg

et al. 2003

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“…The progression to chronicity and complication is directly related to high viral replication demonstrable serologically by the presence of markers of pathogenicity and infectivity [11]. These serological markers include Hepatitis B surface antigen (HBsAg), HB anticore antibody (anti HBcIgM and HBcIgG), Hepatitis e antigen (HBeAg), antihepatitis e antibody (anti HBeAb), and HBV DNA [12]). Hepatitis B 'e' antigen reflects high viral replication and infectivity [13,14].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Some Immunological and Haematological Indices of Hepatitis B Infected Subjects in Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria

Francisca¹,

Jc²,

Ifeanyi³

et al. 2017

J Biomedical Sci

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This study was carried out to evaluate some immunological and haematological indices of HBV infected subjects in Nnamdi Azikiwe University Teaching Hospital, Nnewi. A total of 150 blood samples were collected from confirmed HBV positive subjects that have tested negative to HIV and HCV and consisted of (65 males) and (85 females) with average age of 35 years. A 102 apparently healthy subjects (controls), consisted of (58 males) and (44 females) with average age of 35 years. The investigations for positive and control subjects were done using standard methods. Haematological parameters were assessed using Sysmex KX-21 N automated counter. CD4 was estimated using Partec CD4 easy count kit with Partec IVD Flow Cytometer. IgG and IgM levels were determined using quantitative turbidmetric method at 540 and 340 nm. Serological markers: HBsAg, HBeAg, HBsAb, HBeAb and HBcAb were determined using one step cassette HBV test kit. Results revealed that there was significant difference between the haemoglobin concentration, monocytes and packed cell volume of hepatitis B infected subjects of different age group (P<0.05). The IgM of the positive subjects was significantly lower than that of the control negative subjects (P<0.05). The IgM of the HbAg positive markers was significantly lower than that of the control negative counterpart likewise the female subjects (P<0.05). The CD4 count, absolute eosinophils count and monocytes count of HbsAg positive subjects were significantly lower than that of the HbAg negative subjects (P<0.05). The absolute eosinophils count of HbAg positive males was significantly lower than that of the control negative subjects (P<0.05). We also discovered that the CD4 count, absolute lymphocyte count and monocytes counts were significantly lower in HbAg positive females than their control counterpart (P<0.05). The haemoglobin concentration, eosinophils count and monocytes count of the HbAg positive subjects was significantly lower than that of the control counterparts. It also revealed high prevalence markers of HBV in the study population as, HBsAg (88%) , HBeAg (30.7%) , HBsAb (4.0%) , HBeAb (8.0%) , HBcAb (13.3%) and high prevalence HBcAb (54.9 %) markers in control negative subjects (P<0.05) . The importance of proper evaluation using all hepatitis B markers for immunological and haematological diagnosis of hepatitis B virus infection cannot be neglected.The result of this study shows the need to include all the serological markers, immunological and haematological parameters in routine diagnosis of HBV infection in Nigeria. It also confirms the fact that testing blood donors for HBsAg alone is not sufficient to eliminate HBV from blood.

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“…Hepatitis-B-Virus (HBV) infection elicits a prominent immune response against hepatitis-Bcore-antigen (HBcAg) [1][2][3][4][5]: IgG-antibodies against HBcAg (anti-HBc) persist lifelong in HBV exposed individuals whereas IgM-antibodies decline becoming undetectable after recovery from hepatitis-B [4,[6][7][8]. Commercial assays for IgM-anti-HBc are proposed for diagnosis of acute-hepatitis-B (AHB) that is based on a clinically standardized threshold of 600 Paul-Ehrlich (PEI) [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…Commercial assays for IgM-anti-HBc are proposed for diagnosis of acute-hepatitis-B (AHB) that is based on a clinically standardized threshold of 600 Paul-Ehrlich (PEI) [6][7][8][9]. Using the analytical sensitivity cut-off of the assays low levels of IgM-antiHBc were found to fluctuate in chronic-hepatitis-B (CHB) paralleling the disease remission and reactivation phases [10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Total hepatitis B core antigen antibody, a quantitative non-invasive marker of hepatitis B virus induced liver disease

Moriconi

Yuan

Song

et al. 2015

Digestive and Liver Disease

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Non invasive immunologic markers of virus-induced liver disease are unmet needs. We tested the clinical significance of quantitative total and IgM-anti-HBc in well characterized chronic-HBsAg-carriers. Sera (212) were obtained from 111 HBsAg-carriers followed-up for 52 months (28-216) during different phases of chronic-HBV-genotype-D-infection: 10 HBeAg-positive, 25 inactive-carriers (HBV-DNA2000IU/ml, ALT<30U/L), 66 HBeAg-negative-CHB-patients and 10 with HDV-super-infection. In 35 patients treated with Peg-IFN ±nucleos(t)ide-analogues (NUCs) sera were obtained at baseline, end-of-therapy and week-24-off-therapy and in 22 treated with NUCs (for 60 months, 42-134m) at baseline and end-of-follow-up. HBsAg and IgM-anti-HBc were measured by Architect-assays (Abbott, USA); total-anti-HBc by double-antigen-sandwich-immune-assay (Wantai, China); HBV-DNA by COBAS-TaqMan (Roche, Germany). Total-anti-HBc were detectable in all sera with lower levels in HBsAg-carriers without CHB (immune-tolerant, inactive and HDV-superinfected, median 3.26, range 2.26-4.49 Log 10 IU/ml) versus untreated-CHB (median 4.68, range 2.76-5.54 Log 10 IU/ml), p<0.0001. IgM-anti-HBc positive using the chronic-hepatitis-cut-off" (0.130-S/CO) were positive in 102 of 212 sera (48.1%). Overall total-anti-HBc and IgM-anti-HBc correlated significantly (p<0.001, r=0.417). Total-anti-HBc declined significantly in CHB patients with response to Peg-IFN (p<0.001) and in NUCtreated patients (p<0.001); the lowest levels (median 2.68, range 2.12-3.08 Log 10 IU/ml) were found in long-term responders who cleared HBsAg subsequently. During spontaneous and therapy-induced fluctuations of CHB (remissions and reactivations) total-and IgM-anti-HBc correlated with ALT (p<0.001, r=0.351 and p=0.008, r=0.185 respectively). Total-anti-HBc qualifies as a useful marker of HBV-induced-liver-disease that might help to PLOS ONE |

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Serological diagnosis of acute viral hepatitis

Cited by 39 publications

References 28 publications

Evaluation of Two New Automated Assays for Hepatitis B Virus Surface Antigen (HBsAg) Detection: IMMULITE HBsAg and IMMULITE 2000 HBsAg

Evaluation of Two New Automated Assays for Hepatitis B Virus Surface Antigen (HBsAg) Detection: IMMULITE HBsAg and IMMULITE 2000 HBsAg

Evaluation of Some Immunological and Haematological Indices of Hepatitis B Infected Subjects in Nnamdi Azikiwe University Teaching Hospital, Nnewi, Anambra State, Nigeria

Total hepatitis B core antigen antibody, a quantitative non-invasive marker of hepatitis B virus induced liver disease

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