Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increases in plasma levels of soluble CD8 (SCD8) antigen and expansion of the CD8+ CD38+ lymphocyte compartment were early immunologic alterations frequently observed prior to detection of antibodies against human immunodeficiency virus type 1 (HIV-1) and diminution of CD4+ cells in subjects at risk to develop AIDS. These increases identified in the 49 seronegative homosexual men were manifest in all 164 homosexual subjects and 45 intravenous drug users (IVDU) positive for HIV-1 antibodies (HIV-1+), 19 patients with ARC, and 29 AIDS patients. Augmentation of plasma sCD8 antigen correlated with increases in both CD8+ and CD8+ CD38+ cells in HIV-1(-) homosexual men (r = 0.35, P less than 0.013; r = 0.48, P less than 0.0005; respectively) and the 258 HIV-1+ subjects (r = 0.25, P less than 0.0003; r = 0.33, P less than 0.0001, respectively). In vitro examination of unstimulated peripheral blood lymphocytes from HIV-1+ homosexuals and IVDU confirmed the fivefold higher constitutive levels of cellular release of sCD8 antigen in these subjects compared to heterosexual controls. Inclusion of radiolabeled amino acids during the 3-day culture period in the presence or absence of phytohemagglutinin resulted in negligible levels of radioactivity associated with the sCD8 antigen indicative of a lack of de novo synthesis. Throughout clinical progression to AIDS, sCD8 antigen levels continued to escalate relative to the numbers of CD8+ cells bearing CD38+ antigen. The data confirm the interrelationship between sCD8+ antigen and CD8+ and CD8+ CD38+ cells.
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PMID:Increases in soluble CD8 antigen in plasma, and CD8+ and CD8+CD38+ cells in human immunodeficiency virus type-1 infection. 161 15

Immunization of AIDS/ARC patients with autologous cells expressing HIV antigens, although providing clinical and biological benefits, fails to restore cellular immunity. The latter result is due partly to the antiproliferative effect of HIV-1 on activated T-cells (immune suppression), which leads to blockade of specific immune reactions. To overcome immune suppression, a new vaccine strategy was designed consisting of an immunization against HIV-1 combined with components of the T-cell-suppressive (antiproliferative) network. This new vaccine treatment proved to be innocuous in mice, monkeys, and two non-HIV-infected humans. A Phase I clinical trial was performed in six patients previously under cellular immunotherapy and still presenting a cellular immune defect. Preliminary results confirmed, after a 1-year follow-up of the patients, the safety of the new vaccine, which also partially restored the cellular immune response, including anti-HIV HLA-restricted cell-mediated cytotoxicity, delayed hypersensitivity to recall antigens, and proliferation of T-cells specifically activated by recall antigens.
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PMID:One-year follow-up of vaccine therapy in HIV-infected immune-deficient individuals: a new strategy. 161 65

The effect of AZT on serum HIV p24 antigen and endogenous serum alpha interferon levels was studied in AIDS and ARC patients. Following administration of AZT there was a rapid decline in the serum levels of both HIV p24 antigen and alpha interferon. When AZT treatment was interrupted, the levels of both HIV p24 antigen and of interferon rapidly increased. These findings suggest that HIV or some other AZT sensitive microorganism is the inducer of interferon which is characteristically found in the serum of AIDS and symptomatic HIV infected patients. They also suggest that the rapid decline in interferon levels may underlie some of the symptomatic benefit that follows administration of AZT.
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PMID:Modulation of alpha interferon levels by AZT treatment in HIV-seropositive patients. 162 38

Despite the presence of activated CD8+ T-cells that have been identified in infected individuals, these cells do not overcome natural HIV infection. To understand this better, we analyzed the CD8+ cell-dependent HIV-specific lymphoproliferation that occurs after HIV infection. Our study group of 36 individuals included 11 asymptomatic and 16 symptomatic patients (12 ARC and 4 AIDS), as well as HIV-seronegative controls. After CD8+ cell depletion of PBMC cultures, the remaining cells were tested for proliferation during culture with a well-defined and immunodominant gp41-derived HIV analog, gp41(8). After CD8+ cell depletion, three functional outcomes, which differed in accordance with the disease status of the individual, were consistently recorded, namely (i) an "abrogation effect," (ii) an "augmentation effect," or (iii) "no effect." First, removal of CD8+ cells from PBMC cultures abrogated gp41(8)-specific lymphoproliferation in gp41(8)-specific responders. Paradoxically, in other patients, including 5 symptomatics, the same inhibition of CD8+ cell function caused significant augmentation of gp41(8)-specific lymphoproliferation. These results suggest that the subpopulations of CD8+ T-cells that predominate at different stages of HIV-induced disease have different functional properties, including the ability to modulate HIV-specific cell-mediated immunity.
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PMID:CD8+ T-cells from HIV-infected patients can either augment or abrogate HIV-specific lymphoproliferation. 164 59

A simple, rapid, reproducible and sensitive peptide-Time-Resolved-Fluoroimmunoassay (TR-FIA) method is described which allows the detection of antibodies to the Human Immunodeficiency Virus type 1 (HIV-1). By using a panel of synthetic peptide antigens that covered env, gag and pol amino acid sequences, a 20 amino acid peptide (GIWGCSGKLICTTAVPWNAS) describing an immunodominant and conserved domain on the gp41 region of the BH10 clone was found to be the most reactive in this study. Optimal conditions for antigen concentration, serum dilution and incubation time were established. The peptide-TR-FIA is specific, as assessed by testing HIV-1 positive sera which included samples from AIDS, ARC patients and HIV-positive drug users. The test was used to detect HIV antibodies in 250 well characterized HIV-1 positive sera and 50 normal sera. Peptide-TR-FIA results indicate that the env peptide was highly reactive with HIV-positive sera showing a sensitivity of 100%. None of the 50 control sera showed positive reactivity against the synthetic peptide. Furthermore the peptide-TR-FIA allowed a fine titration of antibodies to defined epitopes of immunodominant HIV structural proteins that usually cannot be achieved by peptide-ELISA assays.
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PMID:Detection of antibodies to human immunodeficiency virus type I by using synthetic peptides and time-resolved fluoroimmunoassay (TR-FIA). 164 52

The Association of State and Territorial Public Health Laboratory Directors (ASTPHLD), CDC, and other organizations (e.g., American Red Cross [ARC] and Consortium for Retrovirus Serology Standardization [CRSS]) have recommended for antibody testing to human immunodeficiency virus type 1 (HIV-1) that duplicate repeat reactive enzyme immunoassay (EIA) screening results be confirmed by a supplemental test. This report examines the variation in Western blot (WB) interpretive criteria reported by laboratories enrolled in CDC's Model Performance Evaluation Program (MPEP) for HIV-1-antibody testing.
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PMID:Interpretive criteria used to report western blot results for HIV-1-antibody testing--United States. 165 86

Zidovudine use data were examined in the Multicenter AIDS Cohort Study to determine (i) if the proportion of pre-AIDS participants (i.e., CD4+ cells less than 200/mm3 or AIDS-related complex) taking zidovudine is high enough to explain a slower than expected rise in AIDS incidence in U.S. homosexual men since mid-1987; (ii) which factors are associated with starting zidovudine and clinical trials of zidovudine; and (iii) if pre-AIDS patients, as a group, are being undertreated. Data on zidovudine use, clinical trial participation, and sociodemographic, clinical, and hematologic variables were collected every 6 months from 1,195 AIDS-free HIV-1-seropositive homosexual men from April 1987 to September 1989. Overall prevalence of zidovudine use rose from 3.6% in mid-1987 (visit 7) to 23% in mid-1989 (visit 11). Of those with less than 200 CD4+ lymphocytes/mm3, the prevalence of zidovudine use rose from 23% (24% if those taking zidovudine or placebo as part of a clinical trial are included) at visit 7 to 58% (69%) at visit 11. Of those with ARC, 20% (23%) were using zidovudine at visit 7 and 55% (65%) at visit 11. Although numbers were small, the advanced ARC participants (CD4+ cells less than 200/mm3 and two or more symptoms) reported the highest treatment rates (50, 78, 80, 60, and 74% at visits 7-11, respectively). By September 1989, 42% (31%) of those with CD4+ lymphocyte levels less than 200/mm3 were still not receiving zidovudine, suggesting that many high-risk, pre-AIDS individuals are being undertreated. To explore this finding further, we examined a range of sociodemographic, hematologic, and clinical variables to determine which factors best predicted initiation of zidovudine therapy outside of clinical trials. In multivariate analyses, CD4+ lymphocyte number was the most consistent predictor of initiation of therapy over all four study visits. For each 100 cells/mm3 deficit, the odds ratios were 2.3 (95% C.I. of 1.7-3.1) at visit 7 and 1.7% (95% C.I. of 1.4-2.0) at visit 11. Symptom status and education level were also associated with starting zidovudine, but not at all visits. The relatively low predictive power of the clinical variables raises and the possibility that nonclinical factors not measured in the MACS (drug cost, third-party insurance restrictions, and individual preferences) may play an important role in predicting zidovudine use. Finally, comparisons were made between seropositive participants starting clinical trials of zidovudine and the rest of the study population. No important differences were found in demographic or major clinical variables between clinical trial participants and zidovudine nonusers in this study.
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PMID:Zidovudine use in AIDS-free HIV-1-seropositive homosexual men in the Multicenter AIDS Cohort Study (MACS), 1987-1989. 167 11

The pathophysiology of anemia in patients with human immunodeficiency virus (HIV) infection is multifactorial. In order to determine the role of erythropoietin (EPO) response as a cause of the anemia, serum levels were determined by direct radioimmunoassay in 110 symptomatic patients with various stages of HIV infection. Symptomatic patients (ARC and AIDS) not receiving zidovudine (ZDV) therapy demonstrated a strong inverse relationship between serum EPO and hemoglobin levels (p = 0.01 and p less than 0.001, respectively). Patients with AIDS who were anemic while receiving ZDV demonstrated serum EPO levels that ranged from normal to markedly elevated (9-3,390 mU/ml). The diversity of serum EPO levels in patients with HIV infection and anemia suggests that the etiology of anemia in these patients and their potential response to recombinant human EPO may not be uniform.
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PMID:Serum erythropoietin titers in patients with human immunodeficiency virus (HIV) infection and anemia. 154 78

12 cases of peripheral facial nerve palsy in African patients attending the Centre National Hospitalier Universitaire de Bangui, Central African Republic, with HIV infections are described with clinical and serological findings. All sera were tested with ELISA and confirmed with Western blot for both HIV-1 and HIV-2 (ELAVIA 1, ELAVIA 2, LAV BLOT I, LAV BLOT II, Diagnostics Pasteur). All 12 were HIV-1 positive and HIV-2 negative. Clinically, 1 patient met the clinical definition of AIDS, 3 had AIDS-related complex, and 8 had been previously health. In 11 cases, facial nerve palsy was the 1st presenting syndrome of HIV infection. ONset was acute in all, and associated with flu-like symptoms in 7. The palsy resembled Bell's palsy in 9, but was associated with unilateral vesicular eruptions suggestive of Ramsay-Hunt syndrome, or varicella-zoster, in 2 cases. In 1 19-year old woman complete facial paralysis with peri-oral numbness and paresthesia of the cheek developed in 1 hour. All recovered in 2 weeks to 3 months. The T4 lymphocyte counts averaged 764 in the healthy patients and 373 in the ARC and AIDS patients, compared to 1949 in controls. T4/T8 ratios averaged 0.66 and 0.45 in these groups compared to 1.32 in controls. 4 other cases of facial palsy in persons testing negative for HIV are also described. Speculative explanations for the pathophysiology of these palsies were offered: local infection of the facial nerve or ganglion by HIV, inflammatory demyelinating neuropathy, or secondary infection, due to immunosuppression, by agents such as Herpes zoster.
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PMID:Peripheral facial nerve palsy related to HIV infection: relationship with the immunological status and the HIV staging in Central Africa. 168 26

The effects of HIV infection on HBV and HDV replication and liver damage were evaluated by comparing the findings from 48 anti-HIV-positive HBsAg chronic carriers with those from 22 matched anti-HIV-negative subjects. The state of HBV/HDV infection was also related to the degree of immunodeficiency of the anti-HIV-positive patients. Most patients were intravenous drug addicts (IVDA) (84.2%); male homosexuals represented only a small proportion (7.1%). Serum HBV-DNA was detected more frequently in anti-HIV-negative than in anti-HIV-positive patients (50% vs. 35%) despite evidence of HDV replication in the anti-HIV-negative group (P = 0.02). Seroconversion from ongoing to inactive HBV infection occurred in 45% of anti-HIV-negative patients as well as in 23% of anti-HIV-positive patients (P = ns). The difference in severity of liver damage between the two groups was not statistically significant (P = 0.84). Furthermore, in the anti-HIV-positive subjects, HBV and/or HDV activity was detected in 63% of patients with mild immunodeficiency (CDC groups II and III with a total CD4 count greater than 400/mm3) and also in 75% of ARC-AIDS patients (CDC groups IV A-IV C) (P = ns). Severe hepatic disease occurred in subjects with CD4 counts above or below 400/mm3 (13 vs. 6, respectively). In conclusion, the data do not demonstrate that HBV or HDV infections are modified by HIV. The epidemiological background of the patients investigated and the extensive spread of hepatitis viruses in Italy before the appearance of HIV may account for the lack of relationship between HIV and HBV/HDV infections.
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PMID:Lack of HBV and HDV replicative activity in HBsAg-positive intravenous drug addicts with immune deficiency due to HIV. 168 Oct 28


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