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)

In 1987, data from the Centers for Disease Control AIDS data base indicated a 50% prevalence of oropharyngeal Candida infection, a 10% rate of esophageal infection, and .5% rate of bronchopulmonary infection among AIDS patients. Candida-positive blood cultures were found in 13 of 903 AIDS patients, and disseminated Candida infection was ascertained in 11 of 101 post mortem examinations of AIDS victims. 5 of 12 patients with oral Candida infection progressed to AIDS within a 42-week investigation as opposed to only 1 of 17 patients without Candida. In the former group, CD4 counts and CD4/CD8 ratios were also significantly lower. Most infections were caused by Candida albicans. Genital Candida occurs in 5-20% of women in reproductive age. In a study of 66 HIV-infected women Candida vaginitis preceded oral Candida infections which preceded Candida esophagitis. 33 women had vaginal infection, 25 had oral Candida, and 9 had esophageal infection with reduced CD4 counts. Infections of the oropharynx and the vagina are reduced CD4 counts. Infections of the oropharynx and the vagina are treated with amphotericin B, nystatin, miconazole, and clotrimazole. Systemically effective compounds include ketoconazole, itraconazole, and fluconazole, although interactions with rifampicin, phenobarbital, and phenytoin used in HIV treatment occur. Fluconazole is contraindicated in C. glabrata and C. krusei infections as it selects for azole-resistant Candida strains. Iv amphotericin B and fluconazole are used in serious infections when oral treatment is ineffective.
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PMID:Candida infections in AIDS patients. 161 60

Anticardiolipin antibodies (ACA) frequently appear in patients with autoimmune disorders such as systemic lupus erythematosus, and have also been detected in infections, neoplasia, the primary antiphospholipid syndrome, in association with certain medications and also in those patients without apparent disease. Recently, anticardiolipin antibodies were described in connection with acquired immunodeficiency syndrome (AIDS). 84 human immunodeficiency virus (HIV)-infected patients were examined in order to assess the influence of risk factors for HIV infection and of the stage of HIV-1 infection on the prevalence of IgG-ACA in HIV-seropositive patients. 2 groups were created -- 1 composed of 38 asymptomatic HIV-infected individuals and the other of 46 AIDS patients. A control group of 42 healthy HIV-negative blood donors was also studied. All those in the control group were IgG-ACA-negative. Of the 84 HIV-positive patients, 50 were IgG-ACA positive (59.5%) and 34 IgG-ACA-negative (40.5%). None of the HIV-positive individuals presented any thromboembolic phenomena. There were no significant differences with respect to sex, risk factors, and stage of disease when the presence of IgG-ACA in HIV-positive patients was ascertained. ACA does not appear to be a prognostic marker in HIV-1 infected patients; the presence of IgG-ACA is probably related to HIV-1 infection itself and is indicative of impaired humoral immunity in this group. (author's modified)
Infection
PMID:Anticardiolipin antibodies and acquired immunodeficiency syndrome: prognostic marker or association with HIV infection? 164 88

The results of antibody assays for viruses of the herpes group (HSV, EBV, VZV and CMV) and for hepatitis B virus (HBV) were retrospectively evaluated in 439 HIV-seropositive patients classified into different stages of HIV infection. The prevalence of specific IgG, IgM and IgA antibodies in these groups was compared with that of a control group of HIV-negative unselected hospital patients. Antibodies to herpes viruses and HBV were more prevalent amongst HIV-seropositives, especially LAS and AIDS patients than in controls. However, marked differences were found only with CMV-IgG and anti-HBc-IgG, both with a comparatively low prevalence in HIV-negative persons (64.5% and 23.2%). Significantly more seropositives were found among asymptomatic HIV carriers (83.3% and 50%) and still more in patients with full-blown AIDS (95.4% and 82.5%). The increased frequency of CMV and HBV antibodies, already seen in asymptomatic HIV patients reflects their higher risk for sexually transmitted infections. Moreover, IgA antibodies to CMV were detected in 25.4% of LAS and 37.3% of AIDS patients, respectively, but only in 7.6% of the controls. Elevated CMV-IgA titres were found exclusively in HIV-infected persons. The differences in the antibody patterns found in this cross-sectional study may reflect the progression of the HIV disease. However, prospective follow-up studies are required to assess the value of these markers as indicators of prognosis in HIV-infected subjects.
Infection
PMID:Prevalence of antibodies to human herpesviruses and hepatitis B virus in patients at different stages of human immunodeficiency virus (HIV) infection. 165 70

Human immunodeficiency virus type 1 (HIV-1) isolates display differences in a variety of in vitro biological properties, including the ability to infect different cell types, the kinetics of replication, and cytopathicity in the infected cells. Studies with isolates obtained from the same individual over time have shown that these in vitro properties of the viral isolates correlate with pathogenicity in the host. The later isolates, recovered when disease has developed, display a wider cellular host range, replicate rapidly and to high titers in the infected cells, and induce syncytia in these cells. In the present studies, the genomic determinants of these biological properties were defined with recombinant viruses generated between two HIV-1 isolates recovered sequentially from the same individual. The results show that the rate of HIV-1 replication in the HUT 78 T-cell line is controlled by the first coding exon of tat. Infection of T-cell and monocytic cell lines is determined by two specific regions in the envelope gp120, one of which also confers the ability of an isolate to induce syncytia. Amino acid sequence comparison of the regions identified revealed minor differences between the two viral isolates: 2 amino acids in the tat gene product and 10 and 12 amino acids in the two regions of envelope gp120. These data suggest that small changes in the tat and env proteins can have dramatic effects on the pathogenic potential of HIV-1.
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PMID:Host range, replicative, and cytopathic properties of human immunodeficiency virus type 1 are determined by very few amino acid changes in tat and gp120. 165 83

In order to investigate the hypothesis that human cytomegalovirus (HCMV) influences HIV-1 infection of brain cells, we studied primary astrocytes derived from human fetal brains and a neuronal cell line (SK-N-MC). Infection of these cells with two strains of HCMV resulted in expression of immediate early, early, and late antigens and production of infectious virus. HCMV infection of primary astrocytes also led to cytopathic effects and cell death. SK-N-MC cells were infected with HIV-1 strains with or without HCMV. HIV LTR-directed CAT activities and the expression of HIV p24 antigen from the SK-N-MC culture coinfected with both HIV-1 and HCMV were higher than those from the cells infected with HIV-1 alone. The primary astrocytes were cotransfected with HIV-1 proviral DNAs and HIV LTR-CAT with or without HCMV infection. HCMV-infected astrocytes produced greater amounts of CAT activity and higher p24 than the cells transfected with HIV-1 proviral DNAs alone. When both primary astrocytes and SK-N-MC cells were transfected with (a) HIV LTR-CAT alone, (b) HIV LTR-CAT plus HCMV-IE gene, or (c) HIV LTR-CAT plus HCMV infection 2 days before the transfection, both HCMV infection and its IE gene trans-activated the HIV LTR promoter. HCMV-IE gene 2 may play a critical role in trans-activation of HIV-1 LTR.
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PMID:Human cytomegalovirus infection and trans-activation of HIV-1 LTR in human brain-derived cells. 166 29

Infection of monocytes with human immunodeficiency virus type 1 (HIV-1) (strain Ada-M) caused increased levels of leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) in vitro. These two products result from the activities of the two enzymes cyclooxygenase and 5-lipoxygenase. The addition of the sesquiterpenoid hydroquinone Avarol, an HIV inhibitor, strongly reduced the levels of LTB4 and PGE2 via inhibition of both cyclooxygenase and lipoxygenase in monocytes. The 50% inhibition concentrations (IC50) for the enzymes were determined to be 2.26 microM (cyclooxygenase) and 1.97 microM (lipoxygenase). A 50% reduction of the extent of PGE2 and LTB4 production in HIV-infected monocytes was measured at a concentration of 0.9 microM Avarol, a dose which caused an 80% anti-HIV effect in vitro (50% inhibition of virus release from infected cells: 0.3 microM). We conclude that Avarol inhibits the enzymes cyclooxygenase and lipoxygenase and suggest that, in general, inhibitors of these enzymes are promising anti-HIV compounds.
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PMID:Avarol restores the altered prostaglandin and leukotriene metabolism in monocytes infected with human immunodeficiency virus type 1. 166 47

Investigations included a group 80 asymptomatic drug addicts. They were examined immunoenzyme method aiming at detection infection by HIV, HBV, HCV and HDV. Cases of seropositive HIV results were confirmed by means WB. In 68 examined patients serological evidence of virus HBV was discovered. In 60 of them one also found out coexisting HIV serological markers, in 51 of HCV markers. HDV antibodies were disclosed in 7 cases. Infection with hepatotropic viruses were more frequent in group of HIV(+) drug addicts.
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PMID:[Serological markers of selected viral infections transmitted by parenteral route in drug addicts]. 166 3

Natural killer (NK) cells are a discrete subset of leukocytes, distinct from T and B lymphocytes. NK cells mediate spontaneous non-MHC-restricted killing of a wide variety of target cells without prior sensitization and appear to be involved in initial protection against certain viral infections. Depressed NK cell-mediated cytotoxicity, one of the many immunological defects observed in AIDS patients, may contribute to secondary virus infections. Here we report that clonal and purified polyclonal populations of NK cells, which expressed neither surface CD4 nor CD4 mRNA, were susceptible to infection with various isolates of human immunodeficiency virus type 1 (HIV-1). Viral replication was demonstrated by detection of p24 antigen intracellularly and in culture supernatants, by the presence of HIV DNA within infected cells, and by the ability of supernatants derived from HIV-infected NK cells to infect peripheral blood mononuclear cells or CD4+ cell lines. Infection of NK cells was not blocked by anti-CD4 or anti-Fc gamma RIII monoclonal antibodies. NK cells from HIV-infected and uninfected cultures were similar in their ability to lyse three different target cells. Considerable numbers of cells died in HIV-infected NK cell cultures. These results suggest that loss of NK cells in AIDS patients is a direct effect of HIV infection but that reduced NK cell function involves another mechanism. The possibility that NK cells serve as a potential reservoir for HIV-1 must be considered.
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PMID:In vitro infection of natural killer cells with different human immunodeficiency virus type 1 isolates. 167 64

Infection of the T lymphocyte with HIV results in a cytopathic effect and cell death that has been linked to a selective loss of the helper T-lymphocyte function of the immune system. In addition to acute infection, which leads to cell death, a chronic or persistent infection also occurs. The persistence of these viral reservoirs has been implicated in the progression of HIV infection and AIDS. Rational drug discovery targeted to late-stage events in HIV replication has the potential to yield antiviral agents capable of blocking virus spread by inhibiting the production of infectious virions from these chronic reservoirs. Steve Petteway and colleagues discuss antiviral strategies that target the chronically infected cell, with a focus on HIV protease inhibitors.
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PMID:The chronically infected cell as a target for the treatment of HIV infection and AIDS. 167 79

In order to find parameters which allow the assessment of the clinical state of HIV patients with or without antiviral therapy, viral cultures on lymphocytes and monocytes/macrophages, CD4-cell counts, HIV antigen, beta 2-microglobulin and serum cholesterol were evaluated for their predictive value. As had been shown previously for lymphocytes, the efficiency of viral isolation on macrophages also depends on the disease stage (CDC) of the patients and thus has a high predictive value. A multivariant discriminant analysis showed that the combination of beta 2-microglobulin, viral antigen, CD4+ cell count and HDL cholesterol predicted the outcome of viral cultures with 80% accuracy. While viral antigen, CD4+ cell counts and beta 2-microglobulin had been known, HDL cholesterol deserves further evaluation as prognostic parameter. The analysis of HIV derived from patients with AZT showed a 20-200-fold in vitro drug resistance after seven to 24 months of therapy. DNA sequence determination of such strains isolated from AZT patients over time showed only two of the amino acid exchanges described in the literature for resistant strains and an additional Val60-Ile transition after 32 months of therapy.
Infection 1991
PMID:Markers for HIV-disease progression in untreated patients and patients receiving AZT: evaluation of viral activity, AZT resistance, serum cholesterol, beta 2-microglobulin, CD4+ cell counts, and HIV antigen. 167 19


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