THE e ANTIGEN AND VERTICAL TRANSMISSION OF HEPATITIS B SURFACE ANTIGEN

Beasley, R. Palmer; Trépo, Christian; Stevens, Cladd E.; Szmuness, Wolf

doi:10.1093/oxfordjournals.aje.a112370

Cited by 565 publications

(256 citation statements)

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“…Early studies suggested a strong correlation between serum HBeAg and high-titer viremia. For instance, it was observed that HBsAg-positive women who were also HBeAg-positive readily transmitted HBV to their newborn, whereas the risk of transmission was much lower if antibodies to HBeAg, rather than HBeAg, were prevalent in the serum [47]. Thus, anti-HBe antibodies appeared to be a Fig.…”

Section: Introductionmentioning

confidence: 99%

Immune selection during chronic hepadnavirus infection

2007

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Purpose Late-stage outcomes of chronic hepatitis B virus (HBV) infection, including fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) result from persistent liver injury mediated by HBV antigen specific cytotoxic T lymphocytes (CTLs). Two other outcomes that often accompany chronic infection, the emergence of mutant viruses, including HBe-antigen negative (HBeAg (-)) HBV, and a reduction over time in the fraction of hepatocytes productively infected with HBV, may also result from persistent immune attack by antiviral CTLs. To gain insights into how these latter changes take place, we employed computer simulations of the chronically infected liver. Methods Computational programs were used to model the emergence of both virus-free hepatocytes and mutant strains of HBV. Results The computer modeling predicted that if cell-tocell spread of virus is an efficient process during chronic infections, an HBV mutant that replicated significantly more efficiently than the wild type would emerge as the prevalent virus in a few years, much more rapidly than observed, while a mutant that replicated with the same or lower efficiency would fail to emerge. Thus, either cell-tocell spread is inefficient or mutants do not replicate appreciably more efficiently than wild type. In contrast, with immune selection and a higher rate of killing of hepatocytes infected with wild-type virus, emergence of mutant virus can be explained without the need for a higher replication rate. Immune selection could also explain the emergence of virus-free hepatocytes that are unable to support HBV infection, since they should have a lower turnover rate than infected hepatocytes.

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Section: Introductionmentioning

confidence: 99%

Immune selection during chronic hepadnavirus infection

2007

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“…Anti-HBc is always present at the onset of disease and reaches a high concentration in sera of patients chronically infected with HBV, but these antibodies do not protect. Anti-HBc passively transmitted to newborns from mothers who are chronic carriers of HBV do not protect these babies from HBV infection (Beasley et al, 1977), indicating that these antibodies do not neutralize the virus. Murray et al (1984Murray et al ( , 1987 and Iwarson et al (1985) demonstrated that immunization of chimpanzees with the core protein of HBV provided complete or partial protection from HBV infection.…”

Section: Introductionmentioning

confidence: 99%

Protection of Woodchucks from Infection with Woodchuck Hepatitis Virus by Immunization with Recombinant Core Protein

Roos

Fuchs²,

Roggendorf³

1989

Journal of General Virology

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SUMMARYWoodchucks were immunized with recombinant woodchuck hepatitis virus (WHV) core antigen (WHcAg) to investigate whether such immunization protects against WHV infection. The C gene was cloned into a pUC12 vector and expressed in Escherichia coll. Core particles purified by sucrose and CsC1 gradient centrifugation had a buoyant density of 1-37 g/ml which corresponded to the density of WHcAg particles present in chronically infected liver. Two animals immunized with the recombinant antigen developed high antibody titres and were protected against infection after challenge with WHV. The surface antigen (WHsAg) and WHV DNA were not detected in the sera of immunized animals after challenge and these animals did not develop anti-WHs. Three control animals developed a typical WHV infection. The protection from WHV infection may depend not on the presence of antibodies against the core protein but on a cellular immune response to WHcAg.

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“…Among pregnant women who are HBsAg carriers there is a high rate of transmission of hepatitis B virus to offspring among those who are e-antigen-positive (Okada et al 1976;Beasley et al 1977). Two of the 4 pregnant HBsAg carriers that we investigated were e-antigen-positive and both, unlike the other 2, who were anti-e-positive, transmitted HBsAg to their children.…”

Section: Discussionmentioning

confidence: 97%

e-Antigen: a link between immune response and infectivity in hepatitis B?

Turner

Green

Blundell

1978

J. Hyg.

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SUTMMARYIn a study of the distribution of e-antigen and anti-e in subjects whose blood was positive for hepatitis B surface antigen (HBsAg), patients with acute hepatitis B who were tested during the incubation period were all e-antigen-positive but after the onset of illness e-antigen was detected in only 11%. Persistence, and in some instances reappearance of e-antigen in those who became long-term carriers of HBsAg was associated with high titres of HBsAg. There was a high incidence of e-antigen in those conditions in which cell-mediated immunity may be depressed, including Down's syndrome and chronic renal failure.The majority of HBsAg carriers identified as sources of infection were e-antigenpositive. A positive reaction for e-antigen is evidently associated with a defective immune response to hepatitis B virus infection which permits continued replication of virus in liver cells accompanied by high titres of HBsAg, numerous Dane particles and detectable DNA polymerase in the blood with consequently a greater likelihood of transmitting infection.Although it cannot be assumed that anti-e positive carriers of HBsAg are not infective, it may be necessary, in the assessment of passive or active immunization for the control of hepatitis B, to take into account the e-antigen/antibody status of possible sources of infection.

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THE e ANTIGEN AND VERTICAL TRANSMISSION OF HEPATITIS B SURFACE ANTIGEN

Cited by 565 publications

References 0 publications

Immune selection during chronic hepadnavirus infection

Immune selection during chronic hepadnavirus infection

Protection of Woodchucks from Infection with Woodchuck Hepatitis Virus by Immunization with Recombinant Core Protein

e-Antigen: a link between immune response and infectivity in hepatitis B?

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