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

We investigated Epstein-Barr virus (EBV)-specific T cell responses in homosexual men with, and at risk for, AIDS. We studied healthy laboratory workers, healthy homosexual men, and patients with AIDS-related complex or AIDS. The cytotoxic activity, absolute number of T4 lymphocytes, and interleukin-2 (IL-2) production decreased, whereas the relative number of Ia+ lymphocytes increased with the extent of infection with the human immunodeficiency virus (HIV). Cytotoxic activity correlated positively with the number of T4 lymphocytes (r = .56, P less than .001) and the amount of IL-2 produced (r = .47, P less than .01) but not with interferon production. Recombinant IL-2, but not gamma interferon, could restore cytotoxic T cell activity to control levels in patients with early HIV infection. EBV-specific serological studies paralleled the T lymphocyte investigations. The increased EBV activity observed in progressive HIV infection may be related to a diminution in the auto-reactive population of the T4 lymphocyte subset and may be amenable to IL-2 reconstitution.
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PMID:Effects of human immunodeficiency virus on the cellular immune response to Epstein-Barr virus in homosexual men: characterization of the cytotoxic response and lymphokine production. 303 Nov 70

The human immunodeficiency virus (HIV)-specific lymphocyte proliferation response was determined for 40 persons at different stages of HIV infection. The specific response to purified HIV virion antigens from strain HTLV-IIIB was poor, occurred in only 9 of the 40 subjects, was not improved with the addition of interleukin-2, and was more frequent in symptom-free individuals (46%) than in patients with lymphadenopathy syndrome (10%). Reactivity to subcomponent p24 was better than that to whole HIV; reactivity was present in five of six infected persons and increased with the addition of exogenous interleukin-2. Reactivities to subcomponents (g)p41 and gp120 were also measured. This is the first evidence of a specific cell-mediated immune response to HIV antigen in HIV-infected persons. Monkeys immunized with purified HIV or with purified p24 displayed cellular immunoreactivity both to whole HIV and to subcomponents. In contrast to the poor reactivity to HIV antigen, the lymphocytes of the patients had good specific cell proliferation responses to cytomegalovirus and herpes simplex virus challenge and a normal response to the addition of phytohemagglutinin. The results suggest a functional defect in peripheral lymphocytes of some HIV-infected individuals on the basis of their response to whole HIV antigen and a better response to gag protein.
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PMID:Characteristics of the specific cell-mediated immune response in human immunodeficiency virus infection. 303 28

The serum levels of a soluble form of the interleukin-2 receptor (sIL-2R) were investigated in 92 patients with human immunodeficiency virus (HIV) infection, ranging from asymptomatic cases to full-blown AIDS. Increased values were found in 69.5% of cases. The overall mean was significantly higher (p less than 0.001) in HIV-infected patients (mean +/- SD = 709.3 +/- 369.4 U/ml) than in the seronegative risk group controls (383.9 +/- 140.5) and normal controls (256.4 +/- 114.5). No major differences were found among the patient groups (asymptomatic infection, persistent generalized lymphadenopathy, symptomatic infection, and full-blown AIDS). These data suggest that the measurement of serum sIL-2R levels may represent a useful biological tool for evaluating T-cell activation phenomena occurring in HIV infection. Since the soluble interleukin-2 receptor maintains the capacity of binding interleukin-2, the increased levels found in HIV infection may play a contributory role towards the in vitro and in vivo impairment of a number of interleukin-2-dependent functions described in this disease. On clinical grounds, the excess of sIL-2R could help to explain the lack of therapeutic effect and little immunological variations following the in vivo administration of interleukin-2.
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PMID:Increased levels of soluble interleukin-2 receptor in the serum of patients with human immunodeficiency virus infection. 312 89

Human immunodeficiency virus type 1 (HIV-1) gene expression is modulated by some virus-encoded proteins, possibly acting at multiple levels of control, which are also known to be involved in the regulation of gene expression in uninfected cells (transcriptional, post-transcriptional, nucleocytoplasmic transport, and translational control). Two anti-HIV-1 drugs, Avarol and 3'-azido-3'-deoxythymidine, which inhibit viral replication by differential mechanisms, were used to study the role of cytoplasmic factors in independent regulation of host cell and viral gene expression. Both drugs were found to inhibit viral replication and synthesis of virus-encoded protein in a synergistic manner, while at cytostatic concentrations, both compounds act antagonistically. ATP-induced transport of viral messengers from isolated nuclei is enhanced by total cytosolic protein from HIV-1-infected cells; a strong increase of the nucleocytoplasmic transport of pol mRNA was measured and, to a lesser extent the transport of certain cellular mRNA (e.g. interleukin-2) was augmented, while the transport of other cellular mRNA (actin) was not affected at all.
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PMID:Differential modulation of host cell and HIV gene expression by combinations of avarol and AZT in vitro. 319 Jul 40

The inhibitory effect on normal natural killer (NK) cell activity of two synthetic peptides corresponding to amino acid sequences 735-752 and 846-860, respectively, as deduced from the amino acid sequences of HTLV-IIIB gp160, was assessed. Sequences 735-752 and 846-860 correspond to regions located within the HIV transmembrane gp41, the carboxy terminus of HIV gp160. These two synthetic peptides have been shown previously to suppress the mitogen- and alloantigen-induced normal human lymphocyte blastogenic responses. Peptides 735-752 and 846-860 conjugated to protein carriers exerted a significant inhibition on the normal NK cell activity assayed against K562 tumor target cells in an in vitro 51Cr-release cytoltoxicity assay. At variance, control peptides similarly conjugated had no effect on NK activity. Addition of exogenous recombinant human interleukin-2 (IL-2) resulted in a partial restoration of the suppression of NK cell activity exerted by both peptides. Binding experiments indicated that peptides 735-752 and 846-860 did not affect the formation of effector cell-target cell conjugates, suggesting inhibitory effect(s) subsequent to the formation of the lytic complex as one potential mechanism of the observed NK suppression. These results suggest that peptides 735-752 and 846-860 homologous to sequences within the HIV transmembrane gp41 may play an important role in the pathogenesis of the defective NK cell activity observed in patients with acquired immunodeficiency syndrome (AIDS).
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PMID:Inhibition of normal human natural killer cell activity by human immunodeficiency virus synthetic transmembrane peptides. 326 Dec 6

Human retroviruses have been detected in supernatants of cultures of Ficoll-enriched lymphocytes from peripheral blood, lymph nodes and bone marrow of (a) 32 out of 42 patients with Acquired Immunodeficiency Syndrome (AIDS), (b) 34 out of 64 patients with AIDS-related Complex (ARC), (c) 9 out of 18 asymptomatic children born from Human Immunodeficiency Virus (HIV) seropositive mothers, and (d) 9 out of 28 asymptomatic drug abusers or hemophiliacs. Virus detection was monitored by assaying culture supernatants for the presence of Mg++-dependent reverse transcriptase (R.T.) activity. A number of these virus-positive sups were passaged repeatedly in cultures of phytohemagglutinin-stimulated and Interleukin-2 (IL-2) treated fresh lymphocytes from healthy blood donors. Occasionally, multiple samples were obtained at varying time intervals from the same patient and consistently yielded detectable retroviral activity. Several isolates were characterized as closely related if not identical to HIV, HTLV-IIIB strain, since cells from either patients' own lymphocyte cultures or subcultures infected with passaged virus were stained in an indirect immunofluorescent assay with both patients sera and monoclonal antibody against p24 antigen of the HTLV-IIIB strain. Representative isolates, grown on fresh lymphocytes of healthy donors and metabolically labelled with 35S-cysteine, were also analyzed in a radioimmunoprecipitation assay (RIPA) against patients' sera to define their antigenic pattern, which was widely superimposable to that obtained with HTLV-IIIB-infected H9 cells. DNA from lymphocytes infected with 2 representative isolates were Southern-blotted and probed with an insert from a plasmid containing the entire genome of the HTLV-IIIB strain. The hybridization patterns were comparable with those obtained with DNA from H9-infected cells.
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PMID:Recovery of HIV-related retroviruses from Italian patients with AIDS or AIDS-related complex and from asymptomatic at-risk individuals. 343 18

A novel, highly quantitative transient expression assay based on the human interleukin-2 (IL-2) gene was used to examine the trans-activation of the Human Immunodeficiency Virus (HIV/HTLV-III/LAV/ARV) long terminal repeat (LTR) in a range of eukaryotic cell lines. In the absence of the trans-activating viral gene product, tat-III, IL-2 transcripts specific for the HIV LTR were present in low abundance in transfected cells and showed a low translational efficiency, when compared with IL-2 mRNAs transcribed from other viral promoters. Coexpression of tat-III resulted in a marked increase in the steady state level of IL-2 mRNAs transcribed from the HIV LTR, and these mRNAs also demonstrated a specific enhancement of their translational efficiency. These results suggest a bimodal mechanism of action for tat-III in the trans-activation of HIV-specific gene expression.
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PMID:Trans-activation of human immunodeficiency virus occurs via a bimodal mechanism. 353 May 1

AIDS is caused by a newly recognised virus (human immunodeficiency virus; HIV) which induces a profound defect in cellular immune function associated with increased susceptibility to opportunistic infections and certain malignancies. The clinical presentation of HIV ranges from asymptomatic infection to severe immunodeficiency manifesting as severe life-threatening infectious diseases or malignancies. While major research efforts are being directed toward development of vaccine and discovery of effective antiretroviral drugs, clinicians are faced with AIDS patients with multiple and complicated medical problems including opportunistic infections and certain malignancies. Currently, efforts are directed toward early diagnosis, treatment, and prevention of recurrence of these opportunistic infections. The current approaches are reviewed in this article. Major recent developments in AIDS research include the isolation of the HIV on culture and the availability of the antibody test. Aside from vaccine and antiretroviral drugs, other measures that may be of benefit in the treatment of AIDS patients are immunological enhancement and reconstitution. Several studies are underway to evaluate antiviral agents in the treatment of HIV infection. Those undergoing clinical trial include suramin, ribavirin, antimoniotungstate, phosphonoformate and azidothymidine. Immune enhancers that have been used include alpha- and gamma-interferon and interleukin-2. HLA-matched lymphocyte transfusions and bone marrow transplantations have been used alone and in combination to replace the AIDS patient's defective immune system.
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PMID:Management of infectious and immunological complications of acquired immunodeficiency syndrome (AIDS). Current and future prospects. 354 66

Human immunodeficiency virus (HIV) infection is associated with abnormalities of both T-cell and B-cell immunity in patients with acquired immunodeficiency syndrome (AIDS). Previous studies demonstrated deficient production of the cytokines interleukin-1 (IL-1), interleukin-2 (IL-2), and gamma interferon (IFN-gamma). Tumor necrosis factor alpha and tumor necrosis factor beta have not been previously investigated in AIDS. In this study we demonstrate that peripheral blood mononuclear cells from patients with HIV infection who have either AIDS-related complex or acquired immunodeficiency syndrome are deficient in the production of tumor necrosis factor alpha and tumor necrosis factor beta. These cytokines, derived predominantly from monocytes or lymphocytes, respectively, function as immunoregulatory, antitumor, and antiinfective proteins. A deficiency in their production may therefore be responsible for many of the complications associated with HIV infection in patients with AIDS-related complex or acquired immunodeficiency syndrome.
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PMID:Tumor necrosis factors alpha and beta in acquired immunodeficiency syndrome (AIDS) and aids-related complex. 369 21

The association of low doses of interleukin-2 (IL-2; 5 IU/ml) and interferon beta (IFN beta; 10 IU/ml) induced an additive or synergic stimulatory effect on natural killer (NK) activity (32%) in peripheral blood samples from hairy-cell leukemia patients, both those with active disease and those in remission. The synergic NK stimulatory effect was more commonly found in samples from patients with active disease, while the additive effect was more frequent in the patients in remission. The IL-2/IFN beta combination provoked a nonadditive nonsynergic NK-stimulatory effect in a further 19.8% samples. The targets of the IL-2/IFN beta combination were typical NK cells, as shown by the fact that there was increased cytotoxicity (synergic, additive or nonadditive nonsynergic) against the K562, but not the Daudi cell line in peripheral blood mononuclear cell samples treated with the combination of the two cytokines. When CD16+/CD56+ or CD57+/CD16+/CD56+ cells were removed, the NK-stimulatory effect was lost. The fact that the NK-cell-enhancing activity of the IL-2/IFN beta combination was reduced when Percoll fractions 2 and 3 were used, but still persisted in 66% of tests, may have been due to cytotoxicity being higher in the untreated fractions 2 and 3 than in the untreated unfractionated samples. One of the factors responsible for the NK-stimulatory effect appears to be the capacity of the IL-2/IFN beta combination to trigger an increase in IFN gamma synthesis. If similar experiments give like results in samples from patients suffering from other B-cell lymphoproliferative, or HIV-associated disorders, all of which are characterized by a deficiency in NK activity, it should be possible to use low-dose IL-2/IFN beta to treat these disorders and, perhaps, residual neoplastic disease without exposing the patient to undue toxicity. Further, by testing other combinations one should be able to identify the lowest IL-2 and IFN beta doses that would effectively boost the additive or synergic effect in a greater number of cases.
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PMID:Natural-killer-stimulatory effect of combined low-dose interleukin-2 and interferon beta in hairy-cell leukemia patients. 751 88


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