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

Lymphocytes expressing interferon-gamma (IFN-gamma) on their surface were evaluated in 61 patients, all IV drug abusers, infected with human immunodeficiency virus type 1 (HIV-1), and in 85 healthy subjects (61 of whom were blood donors and 24 HIV-1 seronegative IV drug abusers). Data obtained demonstrated that IFN-gamma-expressing T lymphocytes, mostly CD8+ cells, were present in HIV-1-infected patients, and that their percentage, always higher in HIV-1-infected patients than in healthy subjects (p less than or equal to 0.001), increased with progressive stages of HIV-1 infection. At the same time other markers of T-cell activation, namely interleukin-2 receptor (rIL-2), transferrin receptor, and HLA-DR were also found to be positive in some of the HIV-1-infected subjects. The presence in the HIV-1-infected patients of activated CD8+ T cells, which are resistant to HIV-1 infection, may suggest that these cells are able to respond to continuous and progressive viral expression (HIV or/and other viruses) and may be a component of the specific response to HIV-1.
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PMID:Interferon-gamma marks activated T lymphocytes in AIDS patients. 214 13

Previously, we demonstrated that cultures of human peripheral blood lymphocytes (PBL) stimulated with herpes simplex virus type 1 (HSV-1) generate antigen-specific, major histocompatibility complex (MHC) restricted cytotoxic T lymphocytes (CTL) that tend to be CD4+ and restricted to HLA-DR antigens. In this study, we present evidence that when HSV-1 stimulated human peripheral blood lymphocytes (PBL) are cocultured with human immunodeficiency virus type 1 (HIV-1), the generation of CD4+, DR-restricted CTL during the 5-day culture period is inhibited. In contrast, HIV-1 had no effect on either natural killer (NK) activity, or on the unrestricted NK-like killers which are often detected in HSV-1-stimulated cultures after the depletion of CD16+ cells. HIV-1 also failed to inhibit the generation of CTL against Epstein-Barr virus (EBV), a response that principally involves CD8+, CD4-, class I-restricted killers.
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PMID:Inhibition of the in vitro generation of class II-restricted, HSV-1-specific, CD4+ CTL by HIV-1. 215 37

Persistent generalized lymphadenopathy (PGL) is a reactive lymphadenitis affecting HIV-positive patients; furthermore, PGL is often a prodrome of AIDS-related complex and AIDS. In the present review the authors describe the histology and the immunohistochemistry of lymph nodes of patients affected by PGL. Histologic alterations of lymph nodes with PGL are classified according to three main types: follicular hyperplasia without or with follicular fragmentation, follicular involution and follicular depletion. Immunohistology demonstrates a peculiar infiltration of CD3+/CD4+ and CD3+/CD8+ lymphocytes in germinal centers; CD3+/CD8+ are often grouped in small clusters centered by a newly formed small blood vessel. Accessory follicular dendritic reticulum cells (FDRCs) of germinal centers are characterized by a positive staining for p24 and p19 HIV major core antigens. In germinal centers, FDRCs undergo progressive lysis in follicular involution and in follicular depletion. Other viral antigens, such as EBV, are infrequently seen in lymph nodes from HIV-positive patients. Paracortical areas of lymph nodes are often characterized by prominent postcapillary venule proliferations and by hyperplasia of the endothelial cells which are HLA-DR positive, often p19 and p24 positive, and occasionally express HIV genome. In conclusion, in PGL the histologic changes correlate well with the immunohistologic features; accordingly, PGL might be considered the result of abnormal immune reactions to several stimuli still incompletely known.
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PMID:Immunohistopathogenesis of persistent generalized lymphadenopathy in HIV-positive patients. 219 30

The skin-specific immune surveillance system protects against invading microorganisms and transformed cells expressing tumor-specific neoantigens. This system includes antigen-presenting Langerhans cells, dermal and epidermal T lymphocytes, cytokine-producing keratinocytes, and draining peripheral lymph nodes. In patients infected with human immunodeficiency virus-1 (HIV-1), this surveillance system appears to be compromised, as evidenced by a reduction in the epidermal Langerhans cell population. Because human epidermal Langerhans cell express surface-bound CD4 antigens, HLA-DR antigens, and Fc-IgG receptors, all of which are involved in HIV-1 binding to, or entry into, the target cell, the reduction in Langerhans cells in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) may be a direct consequence of HIV-1 infection and subsequent injury to Langerhans cells. Detailed ultrastructural studies have confirmed moderate to severe morphologic damage in some Langerhans cells of such patients and the presence of HIV-1-like particles on Langerhans cell surface membranes and in the extracellular spaces. The biologic consequences of Langerhans cell infection by HIV-1 could be either impaired antigen presentation function of viable Langerhans cells or possible transmission of the retrovirus to the T-cell compartment in skin or lymph nodes, with subsequent depletion of CD4+ T cells via widespread syncytia formation between HIV-1-infected and noninfected cells. The facts that herpes simplex virus, specific cytokines, and ultraviolet B radiation can activate signals for HIV-1 expression and that epidermal cells can elaborate large amounts of cytokines, particularly with enhanced ultraviolet B exposure, may have important clinical implications for HIV-1-infected patients.
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PMID:Langerhans cells in HIV-1 infection. 219 48

In ten HIV-infected patients oral hyperpigmentations (HP) were observed, which seemed to be unrelated to any of the known endogenous or exogenous etiological factors. Light microscopy revealed accumulation of Fe-negative pigment in keratinocytes of the stratum basale as well as extra- and intracellularly within the subepithelial connective tissue. The ultrastructure of HP was characterised by the occurrence of melanosomes and premelanosomes within keratinocytes, melanocytes, macrophages and occasionally in fibroblasts, while especially in keratinocytes of the superficial cell layers immature melanosomes were found. Immunohistochemical examination pointed to an increase of HLA-DR positive cells and an altered distribution pattern of immunocompetent cells within the hyperpigmented mucosa. The finding of oral HP in HIV-infected patients may occur due to an increased activity of melanocytes, an increased production of melanosomes and their increased transfer to keratinocytes.
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PMID:[Hyperpigmentation of the oral mucosa in HIV infection]. 223 62

HIV-1, strain HTLV-III, propagated in H9 cells and purified by sucrose gradient centrifugation, was used as native antigen source for the preparation of immunostimulating complexes, HIV-iscoms. The major antigen detected in the iscom was the cell-derived HLA-DR, which readily could be removed from the virus lysate by immunosorbent. In the iscoms the HIV structural proteins MA p17, p55 and TM gp41 were identified; SU gp120 was present in only minute amounts in the virus lysate. The iscom particles appeared well preserved after freeze drying with a round shape, approximately 35 nm in diameter, comprising morphological subunits, assembled with icosahedral symmetry. Immunization experiments in mice reflected the antigen content of the iscoms. High antibody response was induced to HLA-DR in non-depleted iscoms. Major humoral responses were observed to the viral structural proteins MA p17, CA p24, p55, and also to TM gp41. A low or negligible antibody response to SU gp120 was induced by the HIV-iscoms. The negligible response was, however, overcome by the addition of recombinant gp160 to the virus lysate prior to formation of iscoms, resulting in a preparation evoking a clear serum antibody to gp160.
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PMID:Characterization of immunostimulating complexes (ISCOMS) of HIV-1. 225 52

Lymphoid neoplasms associated with acquired immune deficiency syndrome (AIDS) are mostly of B-cell type and rarely of T-cell origin. The authors report a case of a homosexual HIV antibody-positive, HTLV-1 antibody-negative man who developed T-lymphoproliferative disorder (TGLD) after he experienced a viral-like illness. The lymphoproliferative disorder was characterized by increased peripheral blood large granular lymphocytes (LGL) with azurophilic granules (natural killer [NK] cells) which had limited antigen expression: CD2+, CD3-, CD4-, CD8-, CD16+, NKH-1-. The LGL failed to express T-cell or T-cell-related antigens, with the exception of CD2. No functional or gene rearrangement studies were performed on the patient's lymphocytes. However, the results of immunophenotyping, including CD25, W26, and HLA-DR, were suggestive of an inactive state, and the negative finding for CD3 antigen was consistent with unarranged gene T-cell receptors. This is the first reported case of TGLD in an HIV antibody-positive patient.
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PMID:Expansion of large granular lymphocytes (natural killer cells) with limited antigen expression (CD2+, CD3-, CD4-, CD8-, CD16+, NKH-1-) in a human immunodeficiency virus-positive homosexual man. 234 8

We have investigated the features and distribution of accessory cells (ACs) and the relationship of these cells to each other and to lymphocytes in the epithelium and lamina propria of oral hairy leukoplakia (HL), with the objective of better defining the differentiation and mutual interactions of immune-response cells within HL as a preliminary step to understanding the onset and significance of this lesion during human immunodeficiency virus (HIV) infection. Twenty-four HIV-infected patients with HL, two asymptomatic HIV-positive subjects, and three HIV-negative subjects were studied by immunohistochemistry; five HIV-positive patients with HL and three asymptomatic HIV-positive subjects were studied by electron microscopy. In both the epithelium and the lamina propria of HL, we found cells with the immunohistochemical and ultrastructural features of variably differentiated ACs; differences were found between the epithelium and lamina propria. In the lamina propria, ACs were characterized by dendritic shape, multiple contacts with lymphocytes, expression of CD1a antigen, and ultrastructural features of fully differentiated ACs. Conversely, in the epithelium ACs showed bluntly dendritic shape, low expression of CD1a, absent expression of HLA-DR, constant expression of CD11c and CD14 antigens, only occasional contacts with lymphocytes, and ultrastructural features of variably, but always incompletely, differentiated cells of monocyte-dendritic lineage. Seventy-nanometer wide intracisternal particles, closely resembling A particles described in retroviral infections, were found in the intraepithelial ACs in two patients with HL. The defective differentiation of ACs in the epithelium of HL--possibly influenced by the perturbation of the epithelial microenvironment induced by Epstein-Barr virus, and following the direct HIV infection of these cells--and the exceptional finding of close contacts with lymphocytes suggest that the lesional epithelium of HL may constitute a pathway for the entry of foreign antigens which circumvent monitoring by ACs and can induce immune tolerance. The impairment of the local immune response in HL may contribute to the development of full blown, systemic immunodeficiency.
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PMID:Morphology and membrane antigens of nonlymphoid accessory cells in oral hairy leukoplakia. 239 34

Immunoelectron microscopy was applied to study the antigenic make-up of human and simian immunodeficiency viruses (HIV, SIV) grown in cells expressing either MHC class I (Molt-3) or MHC class I and II (H9) antigens. A variety of antibodies directed against the surface glycoprotein gp120 of HIV and against MHC class I and II antigens were employed. Consistent with earlier observations on the loss of HIV envelope components, gp120 was only weakly demonstrable on the mature virion. MHC class I determinants were present regularly in small amounts on HIV and SIV. Class II antigens, e.g. HLA-DR were found in high density on HIV and SIV grown in H9 cells, but were absent, as expected, on virus grown in Molt-3 cells. These cellular surface antigens are constituents of the virion. The presence of MHC class II antigens in virus preparations used for diagnostic purposes might explain some of the false positive results in HIV serology. Possible biological implications of these virus associated cellular antigens for the pathogenicity of HIV are discussed.
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PMID:MHC-antigens: constituents of the envelopes of human and simian immunodeficiency viruses. 245 27

Langerhans cells (LC) are dendritic epidermal antigen-presenting cells expressing the surface molecule CD4, which renders them theoretical cellular targets for direct infection by the human immunodeficiency virus (HIV). To date, somewhat conflicting results have been reported concerning the in vivo infection of LC by HIV as well as the numerical alteration of these cells in the course of HIV infection. In the present work we studied clinically normal skin of a group of 44 HIV-1-seropositive patients classified according to the Centers for Disease Control (CDC) stages II (n = 14), III (n = 9), and IV (n = 21). Monoclonal antibodies (MAb) to HIV p18, p24, and gp120 and to HLA-DR and CD1a antigens (specific for LC) were applied on frozen skin sections using an amplification biotin-streptavidin-fluorescein technique. The MAb to HIV p18 cross-reacted with a cytoplasmic antigen of epidermal basal keratinocytes also present on HIV-seronegative skin specimens. No other reactivity was observed with any of the three anti-HIV MAb. The quantitative study showed that no significant correlations could be established between the number of LC (evaluated independently by HLA-DR and CD1a antigens) and the number of peripheral blood CD4+ve lymphocytes or the CDC disease stage. These results cast some doubt on the previously reported in vivo infection and numerical decrease in LC in HIV infection. The precise involvement of LC in HIV infection awaits further investigation.
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PMID:Immunohistochemical study of normal skin of HIV-1-infected patients shows no evidence of infection of epidermal Langerhans cells by HIV. 247 43


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