The widespread use of Highly Active Antiretroviral Therapy (HAAT) has decreased the progression to AIDS and death (Palella et al., 1998; Porter et al., 2003). In developed nations, the utilization of HAART has rolled out it conceivable to improvement the regular history of HIV contamination into an unending illness that now requires long-term antiretroviral treatment (Mahungu et al., 2009b). Despite the advantages of HAART, wide intraand inter-subject variability has been watched both in light of treatment and in the adverse reaction of certain antiretroviral drugs. In point of fact, reaction to HAART is profoundly complex and frequently restricted by the advancement of short or long term toxicities and the rise of antiretroviral drug resistance. This variability can be clarified by Pharmacokinetics (Factors that manage the availability of the drugs), pharmacodynamics (the effect of drug on the host) and viral pharmacodynamics (the activity of the virus itself).

The efficacy of therapy is influenced by viral sensitivity to a medication. Mutagenesis is a consistent procedure in the viral genome; thusly, mutations happen at every replication cycle, in this manner empowering the infection (virus) to easily adapt. Besides, transmitted HIV drug resistance is a developing phenomenon with vital clinical implications that can bargain initial antiretroviral treatment. Additionally, to viral mutations, different factors may likewise add to treatment failure. Poor adherence is prone to be the most vital reason for treatment failure, however inter-subject variability in pharmacokinetics also assumes to be a vital part. Actually, interindividual variability in the pharmacokinetics of antiretroviral medications can assume a part in treatment failure or toxicity, either straightforwardly, on the grounds that subtherapeutic drug levels can expand the risk of a poor virologic reaction, or in an indirect way, when high (toxic) drug levels produce critical intolerability, prompting poor adherence (Cressey and Lallemant, 2007). Variability between patients in connection to the distribution and bioavailability of antiretroviral drug regimens is most likely determined by genetic and environmental factors, for example, drug-food interactions, drug-drug interactions, sex, and body weight. Specifically, genetic polymorphisms and drug-drug interactions in drug-metabolizing enzymes and drug transporters add to wide variability in drug pharmacokinetics, response to treatment, and lethality (toxicity).

This review provides an overview of pharmacogenetics generally and of current knowledge on pharmacogenetic factors that are connected with both the host and the target (i.e., the infection), which may represent intra-and interindividual variability in responsiveness to antiretroviral treatment. Specifically, this article looks to provide a sup