|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
Notably, a growing body of evidence has recently begun to indicate a protective role for HLA-C in HIV-1 infection, which may suggest that despite the fact that levels of HLA-C expression on both uninfected and HIV-1-infected cells are lower than those of HLA-A/B, HLA-C still presents epitopes to CD8<sup>+</sup> T cells effectively.
|
31217245 |
2019 |
|
HIV-1 infection
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
According to this model, individuals with low-expression HLA-C alleles and unstable binding to β<sub>2</sub>m/peptide might have worse control of HIV-1 infection and an intrinsically higher capacity to support viral replication.<b>IMPORTANCE</b> Following HIV-1 infection, some people advance rapidly to AIDS while others have slow disease progression.
|
29070683 |
2018 |
|
HIV-1 infection
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We evaluated the distribution of HLA-C (rs10484554, rs9264942) and ZNRD1 (rs8321) and ZNRD1-AS1 (rs3869068), single nucleotide polymorphisms (SNPs) in 266 HIV-1-infected and 223 unexposed-uninfected individuals from Northeast Brazil and their relation to HIV-1 infection, CD4 T cells count and viral load pre-treatment.
|
28494720 |
2017 |
|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
Certain Major Histocompatibility-I (MHC-I) types are associated with superior immune containment of HIV-1 infection by CD8+ cytotoxic T lymphocytes (CTLs), but the mechanisms mediating this containment are difficult to elucidate in vivo.
|
28787455 |
2017 |
|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results identify a novel relationship between HLA-C and KIR2DL(+) NK-cell subsets and demonstrate that HLA-C-mediated licensing modulates NK-cell responses to primary HIV-1 infection.
|
25043727 |
2014 |
|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
The emerging role of HLA-C in HIV-1 infection.
|
21896007 |
2011 |
|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
We examined the frequency, function, and phenotype of HLA-C-restricted CTL in ten antiretroviral therapy-naïve Caucasian and African individuals with chronic HIV-1 infection (for at least 8 years; CD4 cell counts in the range of 50-350) who carried the HLA-Cw04 allele.
|
20104487 |
2010 |
|
HIV-1 infection
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here, we show that soluble molecules of the nonclassical major histocompatibility complex class Ib (MHC-Ib) antigen HLA-G are highly upregulated in the plasma during progressive HIV-1 infection, while levels of membrane-bound HLA-G surface expression on dendritic cells, monocytes, and T cells only slightly differ among HIV-1 progressors, HIV-1 elite controllers, and HIV-1-negative persons.
|
20702625 |
2010 |
|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
With its unique specificity for domain 2 of CD4, this antibody potently and broadly blocks HIV-1 infection in vitro by inhibiting a postbinding step required for viral entry but without interfering with major histocompatibility complex class II (MHC-II)-mediated immune function.
|
20463063 |
2010 |
|
HIV-1 infection
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Association of HLA-C and HCP5 gene regions with the clinical course of HIV-1 infection.
|
19050382 |
2009 |
|
HIV-1 infection
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Nef alleles from children with non-progressive HIV-1 infection modulate MHC-II expression more efficiently than those from rapid progressors.
|
17502720 |
2007 |
|
HIV-1 infection
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings also illustrate the capacity for repair of attenuating deletions in HIV-1 infection and suggest that a selective pressure for Nef-mediated MHC-I down-modulation and/or enhancement of virion infectivity exists.
|
10608759 |
2000 |
|
HIV-1 infection
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This down-modulation is transient, occurring 18 h after HIV-1 infection of CD4+ PBL and returning to normal expression by 24 h. In CEM-E5, MHC-I down-modulation occurs over the course of days, reaching its greatest decrease (40%) about the time the cells are producing the most virus.
|
2572645 |
1989 |