These drugs serve to block both HIV-1 infection and production of IL-10 and IL-1β in lymphoid tissue, suggesting a novel approach to HIV-1 therapeutics in which both HIV-1 replication and inflammatory signaling are simultaneously targeted.
IL-10-529C/A gene polymorphism might lead to a decreased risk of HIV-1 infection (A vs. G genotype model: OR = 0.88, 95% CI = 0.73-1.06, p = .166; GG vs. AA+AG model: OR = 0.94, 95% CI = 0.80-1.11, p = .447; GG+AG vs. AA model: OR = 0.75, 95% CI = 0.61-0.92, p = .005; GG vs. AA model: OR = 0.73, 95% CI = 0.57-0.93, p = .012; AG vs. AA model: OR = 0.74, 95% CI = 0.60-0.92, p = .0.007; GG+AA vs. AG model: OR = 1.11, 95% CI = 0.72-1.71, p = .641).
Plasma levels of TGF β 1 and IL-10 showed an inverse correlation with CD8+ T cell counts and CD4:CD8 ratios in patients with non-progressive HIV-1 infection, while plasma HIV-1 RNA positively correlated with CD4+ T cell counts.
Association of IL-10-promoter genetic variants with the rate of CD4 T-cell loss, IL-10 plasma levels, and breadth of cytotoxic T-cell lymphocyte response during chronic HIV-1 infection.
A new multiplexed PCR-SSP assay to detect IL10 SNPs at positions -1082, -819 and -592 was developed and used to determine genotypes and haplotypes in 244 HIV-1 CRF01_AE-infected northern Thais having a median time since HIV-1 infection of 2.7 years.
To evaluate the effect of host genetics on HIV-NRD, we explored validated AIDS restriction gene variants CCR5Delta32, CCR2-64I, CCR5 P1, SDF-3'A, IL-10-5'A, RANTES -403A, RANTES -28G, RANTES-In1.1C, CX3CR1-249I, CX3CR1-280M, IFNG-179T, MDR1-3435T, and MCP-1364G, each of which has been implicated previously to influence HIV-1 infection, AIDS progression, therapy response, and antiviral drug metabolism, and an IL-10 receptor gene, IL-10R1, in the Longitudinal Study of the Ocular Complications of AIDS cohort.
In African Americans, variants in IL10 and related genes might influence multiple outcomes of HIV-1 infection, especially immunological response to HAART.
An estimated 25-30% of long-term nonprogressors (who avoid clinical AIDS for 10 or more years after HIV-1 infection) can be attributed to their IL10-+/+ promoter genotype.