productive HIV 1 replication in T4 lymphocytes is dependent upon the multiplication and activation of the cells. Much like other antiretroviral drugs, resistance to INI emerges through the selection of mutations in the integrase gene influencing the vulnerability of the disease to INI. More than 40 mutations have now been particularly connected with resistance to INSTIs in vitro and in vivo. Weight to raltegravir e3 ubiquitin in vivo has been associated with 14 mutations, to different levels, however the virologic failure observed throughout the BENCHMRK tests was unambiguously associated with two principal independent genetic trails involving key mutations of residues N155 and Q148. These strains weren’t found in the various studies on integrase polymorphism in INI naive people, confirming their likely role in conferring resistance to the class of drugs. Extra mutations increasing the fitness of the resistant infections were recognized in both paths. Specifically, the G140S mutation rescues a defect caused by the primary mutation Q148H. Phenotypic analysis showed that the existence of the mutation at position 148 together with a number of secondary mutations led to greater weight Chromoblastomycosis to RAL than observed for viruses carrying the mutation N155H. Clonal analysis of the populations in 11 patients with treatment failure on raltegravir showed that no viral clone simultaneously carried mutations in place 148 and 155, indicating the exclusivity and independence of both main pathways. Moreover, a change of resistance report from residue 155 to residue 148 variations might occur due to the higher level of resistance to raltegravir conferred by the pathways associated with residue 148 mutation and the greater instability of the pathways associated with residue 155. A small number of mutations involving E157, residues BIX01294 ic50 E92 and Y143 may represent yet another pathway of resistance. There is some debate about whether the first two of these mutations are true primary mutations for RAL resistance, while the Y143 mutation is shown to confer an actual reduction in susceptibility to the inhibitor. Y143R/C/H mutations occur less frequently and later than the other two mutations. The major IN strains E92Q, Q148K/R/H, N155H and E157Q are highly conserved and subject to similar genetic barriers between sub-types B and CRF02 AG. But, the CRFO2 AG subtype includes a stronger genetic barrier to the order of mutations of deposit G140 than subtype B. Another confirmed that treatment failure on raltegravir occurred more rapidly in people infected with non B sub-type viruses, indicating a possible impact of non B related polymorphisms on the screen to raltegravir. HIV 1 can enter resting T-cells, in lack of cell activation the destiny of the viral genome is uncertain.