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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HLA-A, HLA-B, HLA-C, HLA-Bw4, Bw6 and HLA-DR antigens have been detected on purified seminal cells than spermatozoa (SCnonSz) using specific absorptions. These results contrast with those obtained on spermatozoa, which only express significant amounts of HLA-A and HLA-B antigens, and which may be relevant to explain immunosuppressive alloimmunization in the acquired immunodeficiency syndrome (AIDS).
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PMID:HLA-A, -B, -C, -Bw4, Bw6 and -DR antigens are expressed on purified seminal cells other than spermatozoa. 346 36

In light of the importance of virus-specific CTL in the control of the spread of the AIDS virus, it will be important to assess the generation of these effector cell responses in trials of novel vaccine strategies for the prevention of AIDS virus infections. To facilitate such studies in the simian immunodeficiency virus (SIV)/macaque model for AIDS, we have defined a rhesus monkey SIVmac CTL epitope carboxy terminus to both the CD4-binding and V4 regions of the envelope glycoprotein. We also used one-dimensional isoelectric focusing to characterize the MHC class I molecule of the rhesus monkey that binds this 9-amino-acid SIVmac envelope fragment. Cloning and sequencing of the cDNA encoding this rhesus monkey MHC class I molecule demonstrated that it is a newly described HLA-B homologue, Mamu-B*01. The definition of this viral CTL epitope and its restricting MHC class I molecule will facilitate the use of the SIVmac/rhesus monkey model for studies of envelope-based vaccine strategies for the prevention of AIDS.
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PMID:A MHC class I B locus allele-restricted simian immunodeficiency virus envelope CTL epitope in rhesus monkeys. 753 70

Chimpanzees (Pan Troglodytes) and humans are closely related and belong to the same subfamily, Homininae. The approximately 1.8% genetic difference that exists between humans and the chimpanzees must be responsible for observed differences between these two species. It has been shown that chimpanzees can be infected with HIV, but AIDS has not been reported. Furthermore, the prevalence of autoimmune diseases may be low in this species. For instance, type II diabetes occurs, but type I (autoimmune) diabetes (IDDM), to our knowledge, has not been reported. In humans, susceptibility genes for MG and IDDM have been localized to the region between TNF and HLA-B. This region may also influence the rate of progression to death after HIV infection. We have identified differences in this region between humans and the chimpanzees. As shown by PFGE, the TNF to Patr-B region in the chimpanzees is approximately 130-160 kb shorter than the equivalent in humans. Southern and sequence analyses indicate that the deletions in chimpanzees (insertions in humans) include one copy of CL (approximately 10 kb) and the X sequences (< 30 kb). Obviously, other deletions/insertions (approximately 120 kb) need to be identified. Since CL has been shown to be transcribed, the results imply the lack of the gene or, at least, a different gene copy number in the chimpanzees, and we propose that such differences may be relevant to the observed functional differences. We demonstrate here a strategy to identify critical genes responsible for disease development.
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PMID:Differences in the central major histocompatibility complex between humans and chimpanzees. Implications for development of autoimmunity and acquired immune deficiency syndrome. 830 85

Certain HIV-1 infected humans that do not progress to AIDS have been documented to share particular MHC class I alleles that appear to correlate with long-term survival. HIV-1-infected chimpanzees are relatively resistant to progression to AIDS. Out of a group of 10 chimpanzees with CTL activity and nonprogressive HIV-1 infection, 2 animals with prominent cytolytic CD3+CD8+ T cell responses to HIV-1 Ags were studied in detail. Characterization of these CTL revealed that they contained the granzymes A and B, T cell intracellular Ag-1, and perforin and induced calcium-dependent cytolysis that correlated with the presence of apoptotic nuclei in target cells. These CTL responses were directed against two gagpeptides, which were found to be identical to previously described epitopes recognized in the context of HLA-B27 and HLA-B57 molecules. The latter two restriction elements occur with increased frequency in human long-term survivor cohorts. Phylogenetic comparisons revealed that the chimpanzee restriction elements, Patr-B*02and -B*03, described here do not show any obvious similarity with the HLA-B*27 and -B*57 alleles, suggesting that CTL responses to HIV-1 in distinct primate species may be controlled by different types of HLA-B-like molecules. The CTL responses in these two chimpanzees are directed, however, against highly conserved epitopes mapping across the majority of HIV-1 clades.
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PMID:Conserved CTL epitopes shared between HIV-infected human long-term survivors and chimpanzees. 997 8

Host genetic factors, such as HLA alleles, are important in human immunodeficiency virus (HIV) infection and its progression to AIDS. HLA class I gene products are involved in peptide presentation, and each allele is responsible for presenting a different set of peptides to cytotoxic T lymphocytes. The increase or decrease in the frequency of certain alleles in HIV-1-positive versus control subjects would suggest that alleles play a role in susceptibility to or protection against this viral infection. In the present study, 56 HIV-1-positive patients in Chaco Province, Argentina, were typed for the HLA-A and HLA-B loci, using polymerase chain reaction and sequence-specific oligonucleotide probes. The frequency of alleles A*24, B*18, and B*39 was increased in HIV-1-positive subjects, suggesting that these alleles play a role in susceptibility to HIV-1 infection. Alleles B*44 and B*55 were not found in HIV-1-positive subjects, suggesting that they have a protective effect against the disease. The P values of the alleles B*39 and B*44 were statistically significant (P<.05).
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PMID:HLA class I alleles associated with susceptibility or resistance to human immunodeficiency virus type 1 infection among a population in Chaco Province, Argentina. 1101 Aug 37

Certain HLA-B antigens have been associated with lack of progression to AIDS. HLA-B alleles can be divided into two mutually exclusive groups based on the expression of the molecular epitopes HLA-Bw4 and HLA-Bw6. Notably, in addition to its role in presenting viral peptides for immune recognition, the HLA-Bw4, but not HLA-Bw6, motif functions as a ligand for a natural killer cell inhibitory receptor (KIR). Here, we show that profound suppression of HIV-1 viremia is significantly associated with homozygosity for HLA-B alleles that share the HLA-Bw4 epitope. Furthermore, homozygosity for HLA-Bw4 alleles was also significantly associated with the ability to remain AIDS free and to maintain a normal CD4 T cell count in a second cohort of HIV-1-infected individuals with well defined dates of seroconversion. This association was independent of the presence of a mutation in CC chemokine receptor 5 (CCR5) associated with resistance to HIV-1 infection, and it was independent of the presence of HLA alleles that could potentially confound the results. We conclude that homozygosity for HLA-Bw4-bearing B alleles is associated with a significant advantage and that the HLA-Bw4 motif is important in AIDS pathogenesis.
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PMID:Control of HIV-1 viremia and protection from AIDS are associated with HLA-Bw4 homozygosity. 1130 82

The human major histocompatibility complex HLA has been implicated repeatedly as a regulator of the outcome of HIV exposure and infection. A new study of long-term survivors who naturally depress HIV-1 replication and avoid the signs of AIDS for years after infection suggests that homozygosity for a group of HLA-B locus alleles termed Bw4 confers resistance, ostensibly by regulating natural killer cell-ligand interactions. However, close inspection of the accumulated evidence raises some questions and urges validation of the potential Bw4 effects in additional studies.
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PMID:HLA and AIDS: a cautionary tale. 1153 Mar 15

Natural killer (NK) cells provide defense in the early stages of the innate immune response against viral infections by producing cytokines and causing cytotoxicity. The killer immunoglobulin-like receptors (KIRs) on NK cells regulate the inhibition and activation of NK-cell responses through recognition of human leukocyte antigen (HLA) class I molecules on target cells KIR and HLA loci are both highly polymorphic, and some HLA class I products bind and trigger cell-surface receptors specified by KIR genes. Here we report that the activating KIR allele KIR3DS1, in combination with HLA-B alleles that encode molecules with isoleucine at position 80 (HLA-B Bw4-80Ile), is associated with delayed progression to AIDS in individuals infected with human immunodeficiency virus type 1 (HIV-1). In the absence of KIR3DS1, the HLA-B Bw4-80Ile allele was not associated with any of the AIDS outcomes measured. By contrast, in the absence of HLA-B Bw4-80Ile alleles, KIR3DS1 was significantly associated with more rapid progression to AIDS. These observations are strongly suggestive of a model involving an epistatic interaction between the two loci. The strongest synergistic effect of these loci was on progression to depletion of CD4(+) T cells, which suggests that a protective response of NK cells involving KIR3DS1 and its HLA class I ligands begins soon after HIV-1 infection.
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PMID:Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS. 1213 47

Rapid HIV type 1 (HIV-1) mutation coupled with immune evasion poses a major obstacle to effective interventions. In particular, transmission of HIV-1 from a donor partner (transmitter) to a recipient (seroconverter) with similar antigen-presenting molecules (i.e., human leukocyte antigens, HLA) may favor or expedite viral adaptation to host immune responses. Our PCR-based HLA-A, HLA-B, and HLA-DRB1 genotyping for 115 Zambian couples with documented intracouple HIV-1 (mostly clade C) transmission revealed that single-locus HLA allele sharing ranged from 28 to 36%. Different degrees of allele sharing, at single or multiple HLA loci between donor-recipient pairs, were associated with only modest increases in seroconverter RNA level (+0.04 to + 0.24 log(10) copies/mL, p > 0.25). Thus, partial HLA allele sharing commonly seen in Zambian couples did not appear to confer unequivocal early advantage for viral replication in the newly seroconverting subjects. However, correlation of virus loads in seroconverters with those of their known index partners (adjusted Pearson r = 0.21, p = 0.03) did imply that viral characteristics can independently contribute to variability in plasma virus load.
AIDS Res Hum Retroviruses 2004 Jan
PMID:HLA allele sharing and HIV type 1 viremia in seroconverting Zambians with known transmitting partners. 1500 Jun 95

The highly polymorphic gene products of the classical MHC class I genes in humans (HLA-A, HLA-B, and HLA-C) play a critical role in the immune defense against intracellular infections. Because non-human primates are important models for AIDS vaccine research, rhesus monkeys from a thoroughly pedigreed and serotyped colony were subjected to full-length cDNA analysis of MHC class I gene transcripts. Rhesus macaques express multiple dominant Mamu-A and Mamu-B transcripts (majors) per chromosome, which are characterized by high expression levels. The presence of additional cDNAs with low levels of expression (minors) suggests evidence for transcriptional control of MHC class I genes. Moreover, phylogenetic analyses illustrate that most of the Mamu-A and Mamu-B loci/lineages identified display no or only limited levels of allelic polymorphism. Thus, MHC class I diversity in rhesus macaques is typified by the existence of an unmatched high number of Mamu-A and Mamu-B region configurations that exhibit polymorphism with regard to the number and combination of transcribed loci present per chromosome.
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PMID:Unparalleled complexity of the MHC class I region in rhesus macaques. 1566 97


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