HBsAG POSITIVE REACTIVITY IN MAN NOT DUE TO HEPATITIS B VIRUS

Coursaget, Pierre; Bourdil, C.; Adamowicz, P; Chotard, J.; Mar, I. Diop; Yvonnet, B; Mévélec, Marie-Noëlle; Barres, J.L.; N'Doye, R; Chiron, J.P.

doi:10.1016/s0140-6736(87)91255-4

Cited by 84 publications

(31 citation statements)

References 18 publications

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“…Another explanation for isolated HBsAg-positive results may be the absence of anti-HBc antibody response as a consequence of iatrogenic or acquired immunodeficiency. Occasionally, anti-HBc reactivity is absent in patients with selective immunodeficiency or immunocompromised HBsAg carriers (2,10,19,20,25,(32)(33)(34).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…In the majority of patients with continuous HBV infection in Africa, Spain and Taiwan, the serum markers of HBV infection are positivity for HBs antigen and strong positivity for HBc antibody [9,10]. However, there are rare cases of HBV carriers who are negative for HBc antibody with the exception of patients in the terminal stage, irrespective of the presence of hepatitis; this is Terada/Moriyama/Uchida/Arakawa called HBV2 and results in mild hepatitis [8][9][10]. Kaneko et al [11] found that silent HBV infection with negative serum HBV markers is due to an 8-nucleotide deletion in the X gene coding region and a point mutation in DR2 of HBV DNA.…”

Section: Discussionmentioning

confidence: 99%

“…tis, and is not commonly reported [8][9][10]. We have recently clarified that the so-called silent HBV infection with negative serum markers is caused by the deletion of an 8-nucleotide (nt) sequence in the X gene coding region and a point mutation in DR2 [11].…”

Section: Casementioning

confidence: 99%

Nucleotide Sequence of the Precore/Core Gene and X Gene of Hepatitis B Virus DNA in Asymptomatic Hepatitis B Virus Carriers Who Are Negative for Serum Hepatitis B Core Antibody

Terada

Moriyama²,

Uchida³

et al. 2001

Intervirology

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A hepatitis B virus (HBV) carrier who is positive for hepatitis B surface (HBs) antigen but negative for hepatitis B core (HBc) antibody despite persistent HBV infection, is designated has having hepatitis B virus 2 (HBV2). HBV2 is reported to be induced by mild-grade hepatitis. Patients with HBV2 have been reported in Taiwan and Senegal. In the present study, we determined the nucleotide (nt) sequence of the precore/core gene coding region and X gene region of the HBV DNA sequence in 7 subjects who were positive for HBs antigen and negative for HBc antibody. HBV DNA was detected by nested polymerase chain reaction (PCR). Nested PCR was carried out to amplify the precore/core and X open reading frames (ORFs) of HBV DNA. The second PCR products were sequenced, followed by investigation of nt homology. There were no deletions nor insertions in the nt sequence of the precore/core and X ORFs in the HBV DNA of these 7 patients, and mutations were found only sporadically in the 7 patients. Also, there were no common amino acid substitutions in the examined regions of the amino acid sequence of HBV in the 7 patients, and we could not find a common mutation in the examined regions of HBV DNA that could potentially contribute to the development of negativity for HBc antibody. Thus, it is suggested that negativity for HBc antibody in patients with HBV2 is due to an immune response abnormality in the host.

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“…Some failures seem to reflect rare mutational events, for example in Italy (Carman et al, 1990) and Singapore (Harrison et al, 1991). However, in other parts of the world, such as Senegal (Coursaget et al, 1987), failures are so frequent that mutations alone seem an unlikely explanation for the phenomenon. Therefore, a regional divergence in the primary structure of HBsAg, so that at least a fraction of vaccinees are provided with insufficient cross-protection against the locally prevailing strain, cannot be ruled out as the reason for these failures.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, the Thr to Ser substitution at residue 140 in the HBsAg sequence of group E strains, ayw4, and F strains, adw4, may affect one of the immunodominant loops of the a determinant formed by a disulphide bridge between Cys la9 and Cys 147 (Stirk et al, 1992). Therefore, when attempting to explain the vaccination failures reported from some west African countries such as Senegal (Coursaget et al, 1987), where E strains are common, the presence of the Set 14° substitution within the HBsAg sequence of these strains should be taken into account. A Thr to Ser mutation at residue 140 was also found in one of several HBsAg escape variants encountered in a patient treated with a human anti-HBV monoclonal antibody (McMahon et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Genetic relatedness of hepatitis B viral strains of diverse geographical origin and natural variations in the primary structure of the surface antigen

Nordér

Hammas

Lee

et al. 1993

Journal of General Virology

319

292

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A 681 nucleotide fragment of the hepatitis B virus (HBV) genome was sequenced that corresponded to the complete gene for hepatitis B surface antigen (HBsAg) in 80HBsAg-and hepatitis B e antigen (HBeAg)-positive sera of diverse geographical origins. These and 42 previously published HBV sequences within the S gene were used for the construction of a dendrogram. In this comparison, each of the 122 HBsAg genes was found to be related to one or other of the six previously identified genomic groups of HBV, A to F. The HBV strains within each genomic group showed a characteristic geographical distribution. Group A genomes were represented by 23 strains mainly originating in northern Europe and sub-Saharan Africa. The group B and C genomes, represented by 17 and 28 strains respectively, were confined to populations with origins in eastern Asia and the Far East. The group D genomes, represented by 38 strains, were found worldwide, but were the predominant strains in the Mediterranean area, the Near and Middle East, and in south Asia. Group E genomes, represented by nine strains, were indigenous to western sub-Saharan Africa as far south as Angola. There were indications that the F group, made up of six strains, represented the genomic group of HBV among populations with origins in the New World. Thus, HBV has diverged into genomic groups according to the distribution of mankind in the different continents. As well as giving information on the genetic relationship of HBV strains of different geographical origin, this study also provides information on the primary structure of HBsAg in different regions of the world. Such data might prove valuable in explaining the reported failures to obtain protection with current HBV vaccines.

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HBsAG POSITIVE REACTIVITY IN MAN NOT DUE TO HEPATITIS B VIRUS

Cited by 84 publications

References 18 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

Nucleotide Sequence of the Precore/Core Gene and X Gene of Hepatitis B Virus DNA in Asymptomatic Hepatitis B Virus Carriers Who Are Negative for Serum Hepatitis B Core Antibody

Genetic relatedness of hepatitis B viral strains of diverse geographical origin and natural variations in the primary structure of the surface antigen

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