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A 2006 report by Cole et al described the in vitro selection of resistant virus variants to retrocyclin RC-101 . This drug is a cationic θ-defensin that inhibits HIV-1 entry by blocking 6-helix bundle formation in a similar manner to fusion inhibitors such as T20 and T1249 . The resistant variants that emerged had mutations in HR1 and HR2 of gp41 as well as the CD4 binding domain of gp120 (C4 domain). It was noted that the HR1/HR2 double mutant, but also the HR1/HR2/C4 triple mutant, were not able to adequately infect cells in the absence of RC-101. Addition of RC-101 restored infectivity in a dose-dependent manner. Interestingly, the HR2 mutation is identical to the SKY (N126K) mutation that we reported in the T20-dependent virus .
Recently, a drug-enhancement phenotype was reported for an inhibitor-bound form of the CCR5 co-receptor . HIV-1 infection can be inhibited by small molecules that target the CCR5 coreceptor and one of the most promising drugs is SCH-D (Vicriviroc) . It was demonstrated that the fully SCH-D resistant viruses with mutations in the Env gene, enter target cells by recognition of the SCH-D bound form of CCR5. SCH-D does not inhibit these resistant viruses, and even enhances their infectivity modestly.
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