Hepatitis B Vaccine in Medical Staff of Hemodialysis Units

Szmuness, Wolf; Stevens, Cladd E.; Harley, Edward J.; Zang, Edith; Alter, Harvey J.; Taylor, Patricia E.; Vera, Anita DE; Chen, George T. S.; Kellner, Aaron

doi:10.1056/nejm198212093072403

Cited by 254 publications

(71 citation statements)

References 17 publications

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“…Multiple long-term immunogenicity and efficacy trials of the current licensed hepatitis vaccine have defined a protective anti-HBsAg level as Ͼ10 mIU͞ml (8)(9)(10)(11). In mice fed HBsAgtransgenic potatoes, anti-HBsAg antibodies were first detected 1 week after two doses; the response was increased to a peak value of 103 mIU͞ml 4 weeks after the third dose (Fig.…”

Section: Figmentioning

confidence: 99%

Oral immunization with hepatitis B surface antigen expressed in transgenic plants

Kong

Richter

Yang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

288

196

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Oral immunogenicity of recombinant hepatitis B surface antigen (HBsAg) derived from yeast (purified product) or in transgenic potatoes (uncooked unprocessed sample) was compared. An oral adjuvant, cholera toxin, was used to increase immune responses. Transgenic plant material containing HBsAg was the superior means of both inducing a primary immune response and priming the mice to respond to a subsequent parenteral injection of HBsAg. Electron microscopy of transgenic plant samples revealed evidence that the HBsAg accumulated intracellularly; we conclude that natural bioencapsulation of the antigen may provide protection from degradation in the digestive tract until plant cell degradation occurs near an immune effector site in the gut. The correlate of protection from hepatitis B virus infection is serum antibody titers induced by vaccination; the protective level in humans is 10 milliunits͞ml or greater. Mice fed HBsAg-transgenic potatoes produced HBsAg-specific serum antibodies that exceeded the protective level and, on parenteral boosting, generated a strong longlasting secondary antibody response. We have also shown the effectiveness of oral delivery by using a parenteral prime-oral boost immunization schedule. The demonstrated success of oral immunization for hepatitis B virus with an ''edible vaccine'' provides a strategy for contributing a means to achieve global immunization for hepatitis B prevention and eradication.

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Section: Figmentioning

confidence: 99%

Oral immunization with hepatitis B surface antigen expressed in transgenic plants

Kong

Richter

Yang

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

288

196

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“…What we do not know, is whether this cross-reactive T cell response alone yields any protection against a HBV infection. But because HBsAg vaccinations are a very effective measure against a new infection [25,26] , it seems that a concurrent B cell response (i.e. protective anti-HBsAg titer) is primarily necessary to prevent HBV replication.…”

Section: Weihrauch Mr Et Al T-cell Response In Hepatitis Bs Non-respmentioning

confidence: 99%

T cell responses to hepatitis B surface antigen are detectable in non-vaccinated individuals

Weihrauch¹,

Bergwelt‐Baildon²,

Kandic³

et al. 2008

WJG

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CONCLUSION:Our data suggest that there is no general immune deficiency in non-/low-responders. Thus, we hypothesize that the induction of anti-HBsAg responses by vaccination is significantly dependent on the pre-existing T cell repertoire against the specific antigen rather than the presence of a general T cell defect. INTRODUCTIONWorldwide, hepatitis B virus (HBV) infections are a growing problem with a high prevalence of over 8% hepatitis B surface antigen (HBsAg) positive individuals in Africa, South America, parts of Eastern Europe, South Asia, and Canada [1] . It is estimated that approximately 350 million people are chronic carriers of HBV with 1-1.5 million dying from liver cirrhosis and primary liver cancer [2] . Nowadays, protective repeated vaccinations with recombinant HBsAg are not only recommended to all health care workers and travellers, but have recently been included in the childhood and adolescence immunization schedule. Hepatitis B vaccinations prevent HBV infections as well as its complications in most of the vaccines [3,4] . However, 5% to 10% fail to produce protective anti-HBsAg titers after three vaccinations irrespective of the source of the antigen, which is a problem not only for health care workers, and represents a major medical as well as economic challenge [5][6][7] . Low-(HBsAg titer 10-99 kU/L) or Abstract AIM: To evaluate, whether humoral hepatitis-B-vaccine non-responders also fail to mount a T cell response and to compare these results to normal vaccines. RAPID COMMUNICATION T cell responses to hepatitis B surface antigen are detectable in non-vaccinated individuals

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“…Antibodies to the 'a' determinant confer protection against all subtypes of HBV. 8 Mutations in the HBV S gene have been reported in OLT recipients who developed HBV reinfection despite prophylaxis with monoclonal or polyclonal hepatitis B surface antibody (anti-HBs). McMahon et al found amino acid substitutions in the 'a' determinant in all three patients who were reinfected despite monoclonal anti-HBs prophylaxis, 9 while the incidence of mutations in the 'a' determinant in OLT recipients who were reinfected despite HBIG prophylaxis varied from 0% to 33%.…”

mentioning

confidence: 99%

Hepatitis B virus S mutants in liver transplant recipients who were reinfected despite hepatitis B immune globulin prophylaxis†

Ghany¹,

Ayola²,

Villamil³

et al. 1998

Hepatology

307

225

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Early studies found that orthotopic liver transplantation (OLT) for hepatitis B virus (HBV)-related liver failure was associated with a very high rate of reinfection and severe and rapidly progressive liver disease, resulting in a significant decrease in graft and patient survival compared with patients transplanted for other causes of liver disease. 1,2 Various measures have been tried in an attempt to reduce the rate of reinfection. The most promising results have come from the use of long-term (Ն 6 months) high-dose hepatitis B immune globulin (HBIG). 3,4 However, this regimen is expensive, and a significant reduction in the rate of reinfection is mainly seen in patients who have nonreplicative infection pre-OLT. Reinfection despite HBIG immunoprophylaxis may be caused by inadequate neutralization of overwhelming amounts of wildtype HBV, or to breakthrough infection by immune escape mutants.The major B-cell epitopes of hepatitis B surface antigen (HBsAg) have been shown to reside in the 'a' determinant region located at amino acid positions 124-149. 5,6 This region is conformational and is thought to consist of two loops held by disulfide bridges between cysteines 124 and 137, and cysteines 138 and 147. 7 The second loop is more conserved and confers most of the antigenicity of the 'a' determinant; this loop is sometimes referred to as the major hydrophilic region (MHR). HBV can be classified into four major subtypes: adr, adw, ayr, and ayw. Antibodies to the 'a' determinant confer protection against all subtypes of HBV. 8 Mutations in the HBV S gene have been reported in OLT recipients who developed HBV reinfection despite prophylaxis with monoclonal or polyclonal hepatitis B surface antibody (anti-HBs). McMahon et al. found amino acid substitutions in the 'a' determinant in all three patients who were reinfected despite monoclonal anti-HBs prophylaxis, 9 while the incidence of mutations in the 'a' determinant in OLT recipients who were reinfected despite HBIG prophylaxis varied from 0% to 33%. 10-12 Some of these mutations, including the glycine-to-arginine substitution at codon 145, have been shown to decrease binding to monoclonal antiHBs, suggesting that the breakthrough infections were caused by immune escape mutants. 9,11,13 The number of patients cited in the above studies ranged from three to seven patients; therefore, the significance of S escape mutants in HBV reinfection post-OLT remains unclear. It is also possible that additional mutations may be present in the HBV S gene outside the 'a' determinant in patients who received polyclonal anti-HBs (HBIG). Unfortunately, there are very few data on the sequence in the rest of the S gene. In addition, to date, there are no data on the reversibility of these mutations after withdrawal of HBIG therapy.

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Hepatitis B Vaccine in Medical Staff of Hemodialysis Units

Cited by 254 publications

References 17 publications

Oral immunization with hepatitis B surface antigen expressed in transgenic plants

Oral immunization with hepatitis B surface antigen expressed in transgenic plants

T cell responses to hepatitis B surface antigen are detectable in non-vaccinated individuals

Hepatitis B virus S mutants in liver transplant recipients who were reinfected despite hepatitis B immune globulin prophylaxis†

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