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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review the afferent and efferent signals involved in immune signalling at the maternal-fetal interface are highlighted in the light of recent information. MHC antigen expression is reviewed. Immunizing mothers against class I and II MHC antigens can prevent spontaneous fetal resorption in mice. In addition, the CSF family of cytokines is not only secreted in placental tissues, but also play a role in trophoblast proliferation and differentiation. GM-CSF in particular appears to promote trophoblast syncytialization and the synthesis of human chorionic gonadotropin and human placental lactogen. Recent knock-out experiments indicate that CSF-1 is essential for complete fertility. Finally, the fact that the CSF cytokines promote HIV release from macrophages indicates that the knowledge gained in this area could lead to a better understanding of the transmission of the HIV virus from the mother to the fetus through the trophoblast.
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PMID:Immune signalling at the maternal-fetal interface and trophoblast differentiation. 147 93

For a better understanding of the pathogenetic events operative in the cutaneous manifestations of human immunodeficiency virus type 1 (HIV-1) disease, we investigated whether epidermal cells (EC) from HIV-1-seronegative persons can be infected with HIV-1 and, vice versa, whether HIV-1 can be rescued from the epidermis of HIV-1-infected individuals. In a series of three experiments, we consistently found that exposure of EC from HIV-1-seronegative donors to HIV-1 led to viral replication in these cells as evidenced by the detection of HIV-1 p24 in culture fluids. Because EC had been substantially enriched for Langerhans cells (LC) before being exposed to HIV-1, it is reasonable to assume that these CD1a+/CD4+/MHC class II+ antigen-presenting cells of the epidermis represented the actual targets of infection. This assumption is further strengthened by the observation that T cell-depleted cell suspensions from Langerhans cell histiocytosis (LCH) lesions could be productively infected with HIV-1. Conversely, co-culture of epidermal sheets from HIV-1-seropositive individuals with mononuclear phagocytes (MNP) from HIV-1-seronegative donors resulted, after 3 to 5 weeks, in the detection of HIV-1 p24 in 12 of 23 cases. Immunocytochemical analysis, using a monoclonal antibody specific for p24, revealed the presence of HIV-1 in adherent MNP in three cocultures tested. In addition, cellular DNA from these cultures showed strong signals when hybridized to a HIV-1-specific DNA probe. The further finding that two isolates examined exhibited different restriction enzyme patterns indicates that they are separate entities rather than contaminants. Transmission of these isolates to MNP, B- or T-cell lines resulted in cultures strongly positive for p24 and, in the case of H9 cells, for viral particles as detected by electron microscopy. Our results therefore strongly suggest that EC not only can serve as targets for HIV-1, but also can allow efficient virus replication and transmit HIV-1 to various cell types of the hematopoietic lineage.
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PMID:Isolation of human immunodeficiency virus type 1 from human epidermis: virus replication and transmission studies. 151 62

Human T cell glycoprotein CD4 binds to class II MHC molecules and to HIV envelope protein gp120. We have shown that CD4 and synthetic peptides corresponding to amino acid residues 21-49 of the first extracellular domain of CD4, also bind Ig and, with greater avidity, antibody:Ag complex. We investigated the effect of CD4 synthetic peptides on the binding and uptake of human Ig by monocyte/macrophage U937 cells. We found that a synthetic peptide corresponding to amino acid residues 21-49 enhanced binding to U937 cells of both aggregated and nonaggregated Ig. The enhancement was concentration dependent, occurred both in normal and low ionic strength conditions, and varied with the time and the temperature of the preincubation step. The enhancement was maximal after preincubation for 3 h at 37 degrees C. A peptide concentration of 20 micrograms/ml was sufficient for optimal binding of both nonaggregated and aggregated Ig. CD4 peptide 21-49 also enhanced binding of Ig to Staphylococcus aureus protein A. These studies open a new perspective in the way monocyte/macrophage cells handle Ig, antibody:Ag or Id:anti-Id complex, in particular when present at threshold amounts in a nonprecipitating form.
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PMID:Synthetic peptides of human CD4 enhance binding of Ig to monocyte/macrophage cells. I. Characterization and mapping studies. 154 16

In this report we show that signals for transcriptional factors are not restricted to the HIV-1 LTR, but are present throughout the HIV-1 genome. Furthermore, we identified a sequence, AGAACAGATG, highly homologous to the X-box of class II MHC genes and located within the tat-IVS/env region of HIV-1. Double stranded oligonucleotides mimicking the HIV-1 region containing AGAACAGATG were synthesized and band shift experiments were performed demonstrating that this HIV-1 genomic region binds nuclear proteins. We further demonstrate that the binding of nuclear factors to this tat-IVS/env HIV-1 sequence is competed for, in the band-shift assay, by the highly homologous X-box of the promoter of the human HLA-DR alpha gene. The presence in the HIV-1 genome of DNA sequences homologous or identical to regulatory sequences of cellular genes represents a potential mechanism of predation of DNA elements recognized by DNA binding proteins.
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PMID:DNA elements target of transcriptional factors are not restricted to long terminal repeat of human immunodeficiency virus. 156 83

The length of time after which persons infected with HIV-1 progress to AIDS is variable. Certain alleles at the MHC have been shown to influence negatively the clinical outcome of HIV-1-infected persons and to be associated with special clinical manifestations. We investigated the MHC class I, class II and class III antigens in 54 Caucasian HIV-1-infected persons. The MHC profile of individuals with a prolonged period before AIDS is marked by a lower frequency of C4 null alleles.
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PMID:Prolonged clinically asymptomatic evolution after HIV-1 infection is marked by the absence of complement C4 null alleles at the MHC. 157 87

As HIV readily kills CD4 cells in vitro it has been widely assumed that this would account for the declining CD4 counts in vivo. A growing number of reports suggest that the pathogenesis of AIDS is considerably more complex than had been thought. A number of indirect mechanisms for CD4 cell death have been proposed. In this review of alternative theories which could explain the features of AIDS, autoreactivity and genetic restriction to the development of disease are considered the most important. In addition it is suggested that if HIV is able to mimic MHC antigens on the surface of antigen presenting cells then this could stimulate 'allo reactive' T lymphocytes, which would explain the marked similarity of HIV infection to chronic graft versus host disease.
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PMID:The pathogenesis of AIDS: classical and alternative views. 158 22

A new two-step procedure has been developed for the docking of flexible oligopeptide chains of unknown conformation to static proteins of known structure. In the first step positions and conformations are sampled and the association energy minimized starting from an approximate preselected docking position. The resulting conformations are further optimized in the second step by a Metropolis Monte Carlo minimization, which optimizes each of these structures. The method has been tested on the HIV-1 aspartic proteinase complex with an inhibitor, whose crystallographic structure is known at 2.3 A resolution. Furthermore, the application of this method to the docking of the hendecapeptide 58-68 of the influenza A virus matrix protein to the HLA-A2 molecule produced results which are in agreement with experimental observations in identifying side chains critical for T cell recognition and residues responsible of MHC protein binding.
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PMID:Monte Carlo docking of oligopeptides to proteins. 160 11

Depending on the cell line used for virus propagation, human immunodeficiency virus (HIV) particles may possess class II MHC proteins, as demonstrated by FACS analysis. HLA-DR appeared in high amounts at the HIV envelope, if the virus was grown in HLA-DR+ cells, but was absent if the virus had been grown in HLA-DR- cells. No other cellular constituents, including HLA-DQ and HLA-DP, were detected in these virions. The presence of HLA-DR in the virion envelope itself in preparations used for diagnostic purposes may explain some of the false-positive results obtained in earlier serological tests for HIV infection. Possible implications of these virus-associated cellular antigens in the immunopathogenesis of AIDS should be considered.
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PMID:Presence of class II histocompatibility DR proteins on the envelope of human immunodeficiency virus demonstrated by FACS analysis. 160 22

Evidence is accumulating that susceptibility to disease following HIV infection is genetically restricted. In addition, activation of the immune response appears to play an important role in disease progression. Here, John Habeshaw and colleagues propose that HIV envelope glycoproteins mimic foreign MHC molecules and, in doing so, stimulate alloreactive lymphocytes. This activation may explain the marked clinical and immunological similarities between chronic GVHD and AIDS.
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PMID:Does the HIV envelope induce a chronic graft-versus-host-like disease? 162 48

Human T cell lines specific for different peptides of HIV envelope glycoprotein gp120 have been used as probes to identify the availability of functional MHC-peptide complexes on APC. MHC-peptide complexes recognized by T cells specific for peptide 24 (amino acids 225-240) are no longer available on the surface of APC after interaction with irradiated (binding nonproliferating) T cells with the same fine specificity. On the contrary, MHC-peptide complexes recognized by T cells specific for peptide 30 (amino acids 285-300) were functionally available and could stimulate T cells with such a specificity. The reciprocal experiment yielded similar results. The same data were also reproduced with another pair of gp120 peptides. These data demonstrate that upon clustering of peptide-specific T cells with presenting cells presentation of the same peptide to a second cohort of T cells with identical specificity is abolished, suggesting that a selective functional depletion of the MHC-peptide complexes engaged with specific T cells occurs at the surface of the presenting cells. The depletion does not affect other MHC molecules complexed with unrelated peptides.
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PMID:Selective functional depletion of HIV gp120 peptides complexed with MHC from antigen-presenting cells engaged with specific T lymphocytes. 163 69


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