Table 4.

HIV-1 infection of human TH1 clones downregulates IFN-γ expression

CloneaAntigenMean HIV p24 (pg/ml) ± SEM (103)bIFN-γ promoter methylation (fold increase)cIFN-γ RNA expression (fold decrease)d
1 (C01.D6)SEB23,000 ± 11014
2 (H1.15)TTx31,500 ± 2.475>100
3 (H1.12)TTx37,000 ± 2.91520
4 (H1.11)TTx43,500 ± 5.545
5 (H1.18)TTx29,000 ± 3.360>100
  • a T-cell clones were generated, maintained, and activated as described in Materials and Methods. Clones 2 to 5 were from same donor.

  • b Antigen-activated clones were infected with either HIV-1 strain BP-1 (clones 2 to 5) or ADA (clone 1) as described in Materials and Methods. At day 7, medium was removed, stored, and used for HIV p24 assays (data are for triplicates of two experiments).

  • c Determined with a PhosphorImager (Molecular Dynamics) by scanning films of PCR analysis of the methylation status of the IFN-γ promoter SnaBI site. The fold increase was calculated from the integrated volume of the product of the US-AS primer pair normalized to the DS-AS control (see Fig. 4) in the infected clone compared to the paired uninfected clone.

  • d Determined by scanning with a PhosphorImager (Molecular Dynamics) films of RT-PCR analysis of IFN-γ expression; calculated from the integrated volume of the product normalized to the GAPDH internal control product in the infected clone compared to the paired uninfected clone.