The various epistatic effects observed here for common, distinct KIR3DL1 and HLA-B Bw4 combinations are unprecedented with regard to any pair of genetic loci in human disease, and indicate that NK cells may have a critical role in the natural history of HIV infection.
The compound genotype KIR3DS1/HLA-B Bw4-80I, which presumably favors natural killer cell activation, has been implicated in protection against HIV disease.
CCR5delta32 in the context of untreated HIV disease, or HLA-B*5701 allele on the abacavir hypersensitivity reaction in the context of HAART), it is more likely that HIV disease and treatment outcomes are influenced by a multitude of interacting genotypes and phenotypes, a hypothesis that will become increasingly possible to investigate as improvements in molecular and computational technologies are made.
HLA-B*5703 seems to be a protective allele against the progression of HIV infection but could influence the increased incidence of SpA observed in this population.
HLA B*44 is associated with low virus load in human immunodeficiency virus disease, but this association was not evident in this HCV-infected population.
Furthermore, HLA-B gene frequencies in the population are those likely to be most influenced by HIV disease, consistent with the observation that B alleles evolve more rapidly than A alleles.
Although the HLA B(*)5701 class I allele is highly overrepresented among human immunodeficiency virus (HIV)-infected long-term nonprogressors (LTNPs), it is also present at the expected frequency (11%) in patients with progressive HIV infection.
Our findings indicate significant association of pro-inflammatory (IL2, IFN-γ, TNF-α) and anti-inflammatory cytokine gene variants (IL4, IL10) with the risk to acquire the HIV infection and development of AIDS related illness in Indian population.
The follicular phase of the menstrual cycle was associated with an elevated CCL2 level and retention of resident memory CD4+ T cells, which has implications for increased susceptibility to HIV infection.
Dysregulation of IL-2 and IL-7 homeostasis persists in CD4<sup>+</sup>T cell subsets irrespective of presence or absence of viremia or antiretroviral therapy in HIV infection.
However, CD3<sup>+</sup>CD20<sup>+</sup> T cells may also play a protective role in ovarian cancer and HIV infection for their strong propensity to IFN-γ production.
Our findings indicate significant association of pro-inflammatory (IL2, IFN-γ, TNF-α) and anti-inflammatory cytokine gene variants (IL4, IL10) with the risk to acquire the HIV infection and development of AIDS related illness in Indian population.
After adjusting by age, route of HIV infection, length of infection before cART and viral hepatitis coinfection, CCR2 rs1799864-AG genotype was significantly associated with INR status (OR [95% CI]: 1.80 [1.04-3.11]; p = 0.04), and CXCL12rs1801157-TT genotype showed a trend (OR [95% CI]: 2.47 [0.96-6.35]; p = 0.06).
We showed that HIV infection significantly reduced the proportion of Th2 (interleukin 4 [IL-4]/IL-5/IL-13) producing <i>M. tuberculosis</i>-specific CD4 T cells and IL-2-producing <i>M. tuberculosis</i>-specific CD4 and CD8 T cells in individuals with LTBI or PTB (<i>P < </i>0.05).
In this review, we focus on the distinctive and complementary contributions of CCR5 and CCR2/CCL2 in HIV infection, multiple sclerosis, liver fibrosis and associated hepatocellular carcinoma.
Because sICAM1 and CCL2 are associated with an increased risk of HIV-associated neurocognitive disorder, we propose that an established Vpr-ELISA would be useful for monitoring the risk of HIV complications during latent HIV infection.
Past studies on the relationship between Killer cell Immunoglobulin-like Receptor (KIR) and Human Leukocyte Antigen (HLA) genetic variation and chronic immune activation (CIA) in HIV infection are not uniformly consistent.
As a result, CD4+ T cells generally lack effector functions in LNs, including cytolytic capacity and IFNγ and β-chemokine expression, even in HIV elite controllers and during acute/early HIV infection.