undamentally connected with gene substitution in K103N reverse transcriptase while the mutations in Y181C are more commonly emerges with nevirapine treatment (Johnson et al., 2010). A first-generation NNRTI agents has lower genetic barriers for resistance than the second-generation NNRTIs (i.e., etravirine), requiring numerous mutations for loss of movement (Schiller and Youssef-Bessler, 2009).

4.8 ENTRY INHIBITORS
After interaction with the viral receptor CD4 and the co-receptors CCR5 or CXCR4, HIV enters the cell. One of the HIV entry inhibitor, Maraviroc, prevents the usage of CCR5, the co-receptor, and entry of the viral molecule to the targeted cell (MacArthur and Novak, 2008; Donahue et al., 2010). Nevertheless, maraviroc is unable to inhibit the infection with viral molecules which are not CCR5 tropic.

4.9 INHIBITION OF INTEGRATION
Integration is an interesting, unique and fundamental step in viral replication and, for that, it was recognized as a target for medication advancement many years sgo. Nonetheless, raltegravir, is the first integrase inhibitor, which was affirmed by the U.S. Food and Drug Administration (FDA) just in 2007. The postponement was because of the insolubility of HIV integrase and in this way the ability to change its structure and to design inhibitors. Using integrase inhibitors on viral reservoirs effect is still wrangled about.

In addition, the high efficiency of raltegravir has been identified with its great physical-chemical characteristics and it inhibition of the integrase stage in viral replication (Bar-Magen et al., 2010; Donahue et al., 2010). Integrase inhibitors display moderately low genetic barriers for resistance, by which only one or two mutations are able to cause obvious reduction in susceptibility to raltegravir (Delelis et al., 2010; Hatano et al., 2010). In general, the genetic barrier to integrase inhibitors is lower than that off NRTIs. Second-generation integrase inhibitors ar