In the last few years, research in pharmacogenetics and pharmacogenomics has 
identified distinct variants or markers that can help to define the benefits and 
risk of patients requiring antiretroviral treatment. The beneficial effect of 
the deletion 32 allele of the CCR5 coreceptor on the natural history of HIV 
infection and, to a certain extent, on treatment response is well known. The 
bases of immune reconstitution after initiation of antiretroviral therapy, 
although the subject of intense study, are probably multifactorial and 
polygenetic and consequently conclusions with clear applicability to clinical 
practice are currently lacking. Among the risks, no significant progress has 
been made in lipodystrophy. The origin of dyslipidemia associated with 
antiretroviral treatment and the excess cardiovascular risk conferred by some 
antiretroviral drugs is probably polygenetic and, at present, poorly defined. 
The genetic bases of efavirenz-induced neurological toxicity and of 
hyperbilirubinemia secondary to atazanavir are fairly well known, although their 
application in daily clinical practice has not been adequately assessed. Some 
aspects that help to understand the molecular bases of hypersensitivity reaction 
to nevirapine and of nevirapine-induced hepatotoxicity have been described but 
are not applicable in most cases and consequently further studies are required. 
Some data correlate tenofovir-induced renal toxicity with genetic variations in 
some transport proteins. The most significant advance for clinical practice is 
the correlation between the presence of the HLA-B*5701 allele and 
hypersensitivity reaction to abacavir. In particular, one clinical trial with a 
large number of patients from distinct ethnic groups found that the probability 
of not developing hypersensitivity reaction (immunologically confirmed) was 100% 
if the patient was HLA-B*5701-negative. These data suggest the need to implement 
this test in daily clinical practice.