nucleotide) reverse transcriptase inhibitors, as well as thymidine analog mutations, such as TAMs, and non-thymidine mutations, for example, M184V and K65R. In treated patients, TAMs can develop in an organized way, and their accumulation is identified with an increasing level of resistance (Boucher et al., 1992). Commonly, TAMs were chosen by stavudine- and zidovudine-based regimens, yet evidence demonstrates that these mutations are additionally connected to resistance to other NRTI agent (Shafer, 2002).

Actually, there is wide cross-resistance inside the NRTI class. The size of phenotypic and clinical resistance to different NRTIs is by all accounts identified with the number of TAMs. Therefore, particular patterns of TAMs could affect treatment responses differently. In contrast, the K65R mutations are linked with all cross-resistance agents from this class aside from zidovudine. Having low genetic barrier NRTI analogs, have need of a single point mutation to give high levels of resistance, including emtricitabine and lamivudine, while most non deoxycytidine NRTIs, like, didanosine, abacavir, thymidine analogs, and tenofovir (the nucleotide reverse transcriptase inhibitor), are associated with moderate genetic barriers for resistance development.

In spite of the various advantages of NNRTI on virologic results, their utilization is constrained by their low genetic barrier to resistance. First generation of NNRTIs (nevirapine and efavirenz) resistance is described by a quick selection of viruses which have one or a few mutations in the gene of reverse transcriptase that give high level of resistance to these agents. A mutation in the reverse transcriptase enzyme, specifically single-point mutation, is frequently enough to present high-level loss of medication affinity that is connected with significant clinically phenotypic resis