Mechanisms involved in the Abacavir-mediated hypersensitivity syndrome

Cell Res. 2012 Dec;22(12):1637-9. doi: 10.1038/cr.2012.105. Epub 2012 Jul 10.

Abstract

The potentially life-threatening adverse reactions to Abavacir (ABC), a nucleoside analog reverse transcriptase inhibitor for the treatment of HIV infection, have been known for several years to be limited to individuals expressing the HLA-B57:01 gene. Why the ABC hypersensitivity syndrome is only seen in HLA-B57:01-expressing subjects and what the precise mechanisms underlying this intolerance are remain however controversial. A series of recent studies, particularly a study by Illing et al. recently published in Nature, now answer some of these questions and offer new opportunities to better understand autoimmune disorders and prevent adverse reactions to other drugs.

MeSH terms

  • Alleles
  • Anti-HIV Agents / adverse effects*
  • Anti-HIV Agents / pharmacology
  • Anti-HIV Agents / therapeutic use
  • Autoimmunity / drug effects
  • Autoimmunity / immunology
  • Carbamazepine / pharmacology
  • Dideoxynucleosides / adverse effects*
  • Dideoxynucleosides / pharmacology
  • Dideoxynucleosides / therapeutic use
  • Drug Hypersensitivity / etiology*
  • Drug Hypersensitivity / genetics
  • Drug Hypersensitivity / immunology
  • HIV Infections / drug therapy
  • HIV Infections / immunology
  • HIV Infections / metabolism
  • HLA-B Antigens / genetics
  • HLA-B Antigens / metabolism
  • Humans
  • Syndrome

Substances

  • Anti-HIV Agents
  • Dideoxynucleosides
  • HLA-B Antigens
  • HLA-B*57:01 antigen
  • Carbamazepine
  • abacavir