Table 1.
Demographic and clinical characteristics of the population analyzed.
Figure 1.
Restriction fragment length polymorphism (RFLP) analysis of PCR products.
(A) Representative ethidium bromide stained (15%) non-denaturing polyacrylamide gel (PAGE) showing amplified gene product of TNF-α (−238G/A) 118 bp uncut and RFLP pattern observed after digestion with BglII. (Lane M -20 bp ladder, Lane 2 and 8-GA genotype, Lane 3 to 7-GG Genotype. (B) Representative non-denaturing PAGE (15%) showing amplified gene segment of TNF-α (−308G/A) 118 bp uncut and RFLP pattern observed after digestion with NcoI. Lane 1-uncut 118 bp product, Lane 2 and 6-GG Genotype, Lane 3 and 5-GA genotype, Lane 4-AA Genotype, Lane M-20 bp Ladder. (C) Representative non-denaturing PAGE (15%) showing amplified gene segment of TNF-α (−863C/A) 126 bp uncut and RFLP pattern observed after digestion with BsaAI. Lane 1-Negative Control, Lane 2-uncut 126 bp, Lane 3-AA Genotype, Lane 4-CA Genotype, Lane 5, 8 and 9-CC Genotype, Lane 6 and 7-CA Genotype, Lane M-50 bp ladder.
Table 2.
TNF-α genotype and allele frequencies in HCs, HIV-1 infected (FPs+SPs) and ESNs.
Table 3.
Comparisons of TNF-α genotype and alleles in SPs, FPs and ESNs with HCs associations with HIV disease progression.
Table 4.
Observed TNF-α haplotypes and disease progression in HIV-1 patients.
Figure 2.
Plasma concentrations of TNF-α in various study groups.
Plasma concentrations of TNF-α (Mean±SEM) in FPs, SPs and ESNs. High TNF-α producing haplotype CAG (dark bar), medium TNF-α producer haplotype CGG (light gray bar) and low TNF-α producing haplotype AGG (gray bar).
Figure 3.
Plasma viral load and CD4 counts in different TNF-α haplotypes (CGG, CAG and AGG).
(A) Plasma Log10 RNA copies/mL (Mean±Range) in TNF-α haplotypes, CGG (dark bar), CAG (light gray bar) and AGG (gray bar). (B) CD4 counts at different time intervals in TNF-α haplotypes, CGG (dark bar), CAG (light gray bar) and AGG (gray bar). Values shown as (Median±SD). Significance levels: **p<0.01; *p<0.05.
Figure 4.
Gating strategy for the analysis of JC-1 stained PBMCs.
Lymphocytes were gated according to morphological parameters (not shown in figure), JC-1 aggregates and monomers were analyzed on FL2 (PE) and FL1 (FITC) channel respectively, (a) showing JC-1 stained lymphocytes of HCs (P2 gate, 96.4%), (b) protonophore FCCP treated lymphocytes as a positive control showing 84.2% cells having reduced mitochondrial membrane potential. (c) and (d) JC-1 stained lymphocytes in a representative samples from individuals in ‘fast progressors’ group having CGG and CAG haplotypes showing 26% and 37% lymphocytes dying respectively. Change in mitochondrial membrane potential (Δψm) was expressed as percentage of median fluorescence intensity (FL2: FL1/FL2 FCCP: FL1 FCCP) x100.
Figure 5.
Median fluorescence intensities of total lymphocyte mitochondrial membrane potential (Δψm).
Bar diagram showing median fluorescence intensity (MFI) of total lymphocyte mitochondrial membrane potential (Δψm) in FPs and SPs having CAG (n = 5) (dark bar) and CGG (n = 5) (light gray bar) haplotypes (shown as Mean±SEM).