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Table 1 Characteristics of the ten viruses that were used for the in vitro selection experiments

From: HIV-1 protease inhibitor mutations affect the development of HIV-1 resistance to the maturation inhibitor bevirimat

HIV-1 variant

Mutations compared to HXB2

PI resistance

 

Gag

Protease

LPV

ATV

HXB2

-

-

-

-

NL4-3

-

3I-37N

1

1

PR-1

 

3I-20R-35D-36I-54V-63P-71V-82T

12.2

5.6

PR-2

431V

3I-10I-13V-35D-36I-37D-46I-54V-55R-57K-62V-63P-71T-82A-90M-93L-95F

15.1

7.8

PR-3#

431V

3I-10I-13V-35D-36I-37D-54V-55R-57K-62V-63P-71T-82A-90M-93L-95F

> 120

> 120

PR-4#

431V

3I-10I-13V-35D-36I-37D-46I-55R-57K-62V-63P-71T-82A-90M-93L-95F

8.1

11.6

PR-5#

431V

3I-10I-13V-35D-36I-37D-46I-54V-55R-57K-62V-63P-71T-90M-93L-95F

10.8

8.9

PR-6#

431V

3I-10I-13V-35D-36I-37D-46I-54V-55R-57K-62V-63P-71T-82A-93L-95F

19.6

5.9

NC/p1

431V

-

2.6

1.3

NC/p1

436E-437T

-

4.7

3.3

  1. HXB2 and NL4-3 are subtype B reference viruses. Mutations are as compared to HXB2. All amino acid differences in the viral protease are listed. All protease inhibitor (PI) resistance mutations, as defined by the International AIDS Society[37] are in bold. In addition, mutations in the NC/p1 cleavage site are listed. The CA/p2 cleavage site of the ten viruses was identical. PR-1 is clone 460.2 from Nijhuis et al. [21] and PR-2 through PR-6 are the B6 clones from Maarseveen et al. [30]. #PR-3 - PR-6 are site directed mutants created from PR-2. In each of these clones one PI resistance mutation was reverted to wild-type, PR-3 - PR-6 lack PI resistance mutation 46I, 54V, 82A and 90M respectively. The NC/p1 variants only differ from HXB2 at the positions indicated in the table. The level of PI resistance was determined for these viruses against lopinavir (LPV) and atazanavir (ATV). PI resistance is expressed as fold change in EC50 compared to HXB2.