Frequency of HLA B∗5701 allele carriers in abacavir treated-HIV infected patients and controls from northeastern Brazil

Abstract

In clinical practice, using pharmacogenetics has risen in importance since the technologies for genomic variation searches for different responses to drugs became widespread, easier, more rapid, and affordable for a specialized laboratory. The main pharmacogenetics studies have mostly involved drug resistance monitoring in oncology patients;1 however, other applications are being developed to detect genetic molecular markers associated with resistance or hypersensitivity/adverse reactions to antiretroviral drug treatment in Human Immunodeficiency Virus (HIV)-infected patients.2 HIV treatment is known to be limited by adverse drug reactions and the development of resistance. One significant example is the strong association of the Abacavir hypersensitivity reaction with HLA-B*5701 in HIV-positive patients.3 Abacavir, a common drug for treating HIV-infected patients, is an efficient nucleoside reverse-transcriptase inhibitor with a beneficial long-term toxicity profile, often used with other antiretroviral agents. However, Abacavir can yield adverse effects such as immunologically-driven hypersensitivity in 5 to 8% of HIV-positive subjects during the first six weeks of use.2 Hypersensitivity symptoms immediately reverse after the interruption of Abacavir.4 The hypersensitivity reaction to Abacavir has been reportedly associated with the presence of the major histocompatibility complex class I allele HLA-B*5701 and this association has been confirmed in several replication studies in different ethnic groups of HIV-positive patients.3 In our study, we searched for the presence of HLA B*5701 in 96 HIV-positive patients treated with Abacavir and in 243 healthy subjects from Northeastern Brazil (Recife, Pernambuco) to verify the percentage of HLA B*5701 allele carriers in HIV patients and in the general population from Northeast Brazil. This area is known to harbor a tri-hybrid population resulting from contributing African (44%), Caucasian (34%), and native American (22%) genomes.5