Aspectos inmunológicos e inmunogenéticos de la hepatitis B

Evolución histórica

Abstract

The most common cause of viral hepatitis in USA is thc hepatitis B virus, and since 1983 is more common than hepatitis A. In 1980 a serum derived hepatitis B vaccine was evaluated and introduced to clinical practice. The fear of HIV transmission leads to the development in 1984 of a recombinant vaccine produced in the yeast Saccharomyces cerevisae through DNA recombinant technics. Both vaccines have been proved effective and safe, with seroconversion in 85-96% of homosexual males and 96-98% of healthy adults. Several recent studies have shown that 5-10% of healthy adults fail to respond to the vaccine, even after additional dosages.

The mechanism for this lack of Anti-HBs response has been extensively studied by several groups and associated to the major histocompatibility antigens in relationships with T lymphocytes responses to specific antigens. Recent studies have demonstrated that the lack of response to the HBsAg is due to a mechanism of peripheral restriction previously shown by Crave, Alpert et al, and not related to gene suppression nor through CD8T+ cells. The absence of response is secondary to the macrophage-antigen interaction and CD4T+ cells and is also multifactorial. Studies in caucasian populations have shown that poor responders to hepatitis B vaccines have certain haplotypes such as: B8, Dr7, Dr3, Dr7, Dr4 and Dr7+ B8. Alpert et al have shown for the first time in humans that persons homozygous for extended haplotypo, HLA B8-DR3-SC01, have a poor response to a HBsAg and is recessive. Only one haplotype is sufficient to have an adequate Anti-HBs response. Sasasuki et al. in contrast have shown that Japanese haplotype HLA-BW54-DR4-DRW53 and DQW3 is associated to poor response to HBsAg, and is dominant, they also suggest that lack of response depends of an immunosupresion gene through CD8 cells.

Finally our results suggest that no responders have a specific defect located to the level of helper T cells stimulation, and is not mediated through immunosupresion through CD8T cells.