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. 2011 Jan 31;55(4):1806–1809. doi: 10.1128/AAC.01197-10

TABLE 2.

Effect of N348I mutation on RC of molecular clones and clinical isolates in different cell linesa

Subtype Mean % of wild-type RC ± SEM (fold decrease), P value
HEK 293T cells Jurkat cells SupT1 cells
Molecular clones
    p8.9 B 55.57 ± 4.07 (1.80), <0.02 54.16 ± 5.5 (1.85), <0.02 62.91 ± 4.49 (1.59), <0.02
    MJ4 C 34.65 ± 2.28 (2.89), <0.02 23.26 ± 1.57 (4.30), <0.02 26.35 ± 0.44 (3.80), <0.02
    94ug114.1.6 D 68.33 ± 0.94 (1.46), <0.02 67.55 ± 3.03 (1.48), <0.02 73.38 ± 2.66 (1.36), <0.02
Clinical isolates
    A1 42.28 ± 4.39 (2.37), <0.02 31.28 ± 4.28 (3.20), <0.02 37.80 ± 3.49 (2.65), <0.02
    A2 46.86 ± 1.31 (2.13), <0.02 40.25 ± 0.07 (2.48), <0.02 47.46 ± 0.84 (2.11), <0.02
    B 73.20 ± 3.00 (1.37), <0.02 67.12 ± 4.32 (1.49), <0.02 81.92 ± 2.25 (1.22), <0.02
    C 50.39 ± 4.16 (1.98), <0.02 41.87 ± 1.19 (2.39), <0.02 61.17 ± 3.91 (1.63), <0.02
a

Data are from mean RC values for mutant viruses which were calculated from the number of relative light units per nanogram of input p24 and expressed as a percentage of the wild-type value. Fold decreases in RC are shown in parentheses for comparisons of mutant and wild-type values. The standard error of the mean from two independent experiments is shown. Statistical analyses using Student's t test compared the N348I mutant virus with the wild-type virus.