Pathogenesis of antiretroviral drug hypersensitivity reactions

A significant achievement in the field of HIV medicine has been the discovery of pharmacogenomic predictors of antiretroviral drug hypersensitivity resulting from the interactions between drug and class I and/or class II human leukocyte antigen (HLA) molecules.38 Of these,  the association of  HLA-B*57:01 with abacavir hypersensitivity is the best recognised and has resulted in the introduction of testing for HLA-B*57:01 carriage prior to abacavir prescription into routine clinical practice and provided a roadmap for the translation of pharmacogenomics into the clinic. Other described genetic associations with antiretroviral drug hypersensitivity reactions include HLA-C*04:01 with nevirapine-induced SJS and TEN in African people and with DRESS in association with a low nevirapine metabolism status associated with carriage of the CYP2B6 allele of cytochrome P45056, HLA-DRB1*01 with nevirapine rash associated with hepatitis57, efavirenz-induced MPE, and HLA-B*53:01 with raltegravir-induced DRESS.58 Other described associations are outlined in Table 2.