Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In adults with the acquired immunodeficiency syndrome, long-term monotherapy with zidovudine selects for human immunodeficiency virus type 1 (HIV-1) strains with substantially reduced in-vitro susceptibility to the drug. We have assessed the relation between in-vitro resistance to zidovudine and clinical outcome in children, in whom disease progression is more rapid than in adults. We studied 23 children with symptoms of HIV-1 disease during extended monotherapy with zidovudine. An in-vitro assay was used to determine the concentration of zidovudine required to inhibit by 50% the replication of viral isolates (IC50) obtained after 9 to 39 months of treatment. Viral stocks of high enough titre to yield reproducible results were obtained from 19 of the children. During the following 6 months of therapy, 9 children were stable, 7 deteriorated, and 3 died. There was a highly significant relation between decreased zidovudine susceptibility and poor clinical outcome (p less than 0.001) but no relation between IC50 and age at start of therapy or length of time on treatment. Age-adjusted CD4 lymphocyte counts were lower at the start of treatment (p = 0.02) and at the time of sampling (p = 0.01) in children whose viral isolates had an increased zidovudine IC50. Initial serum p24 antigen levels were not predictive of subsequent emergence of resistant virus, but at the time of sampling for viral sensitivity higher p24 antigen levels were associated with raised IC50 (p = 0.004). The findings suggest that most children who become unresponsive to monotherapy with zidovudine, as judged by clinical criteria, will have changes in in-vitro sensitivity to the drug. In these children, an alternative antiretroviral therapy should be considered.
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PMID:HIV-1 sensitivity to zidovudine and clinical outcome in children. 134 39

In studies on viral interference, cloned T-cell lines chronically infected with human immunodeficiency virus (HIV) type 1 or HIV-2 were inoculated with several strains of these two AIDS retrovirus subtypes. HIV-2UC1-infected cells, which still express the CD4 receptor, could be superinfected with a variety of HIV-1 and HIV-2 strains. This event was accompanied by cytopathic effects in the cells and production of pseudotype virions with an expanded cellular host range. HIV-1- or HIV-2-infected clonal cell lines, which did not express CD4, could not be superinfected by any HIV strains but were coinfected after transfection of molecular clones into the persistently infected cells. These observations indicate that viral interference with HIV occurs at the cell surface and involves a down-modulation of the CD4 molecule. If the CD4 protein is expressed, superinfection can take place, and phenotypically mixed virus particles are produced. Since HIV-1 and HIV-2 dually infected individuals have been detected, these in vitro observations may have relevance to the in vivo state.
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PMID:Human immunodeficiency virus (HIV) type 1 can superinfect HIV-2-infected cells: pseudotype virions produced with expanded cellular host range. 134 69

The IgE synthesis is tightly controlled by a complex network of T and B cells. Because human immunodeficiency virus (HIV) disease associates T cell activation and depletion, polyclonal B cell activation, atopic symptoms, drug hypersensitivity, and autoimmune activity, we have evaluated IgE, as well as IgA, IgG, and IgM, in 315 HIV-seropositive individuals with or without acquired immunodeficiency syndrome (AIDS) and compared the results to those of 100 HIV-seronegative subjects. IgE levels were higher in HIV-infected subjects as a whole, compared to levels in seronegative control subjects (p less than 0.05). This difference was particularly marked between patients with AIDS and control subjects (p less than 0.005). A strong relationship appeared between IgE and the immune status as assessed by CD4 cell counts (p less than 0.001 between IgE values in patients with CD4 less than 300 or greater than 300/microliters). In addition, we assessed the predictive value of IgE elevation over disease progression: in subjects with a CD4 count less than 300/microliters, the survival analysis disclosed a 24-month occurrence rate of AIDS of 83% in individuals with IgE greater than 150 KIU/L versus 44% in individuals with IgE less than 150 (p = 0.016). In subjects with an AIDS-related complex, IgE greater than 150 indicated a 100% rate of AIDS versus 9% in individuals with IgE less than 150 (p = 0.003). Thus, IgE levels appear to be a very discriminative marker between patients in late stages of HIV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevation of IgE in HIV-infected subjects: a marker of poor prognosis. 134 48

To examine the immunological changes in cats concurrently infected with feline immunodeficiency virus (FIV) and Toxoplasma gondii, kittens (four per group) were inoculated with FIV, T. gondii, both agents, or no pathogens. Blood mononuclear cells and plasma were collected weekly for lymphocyte assays and serology. At week 14, spleen and lymph node cells were used for lymphocyte assays; brains and mesenteric lymph nodes were used for isolation of T. gondii. More T. gondii organisms were present in tissues of the dually infected cats than in tissues of cats with toxoplasmosis alone. Two dually infected cats and one cat infected with T. gondii developed chorioretinitis. Spleen, lymph node, and blood mononuclear cells from dually infected cats had the greatest reduction in mitogenic responses. By week 3, cats infected with FIV underwent a decrease in the number of CD4 cells that was not changed by concurrent T. gondii infection; the number of CD8 cells increased only in cats infected with T. gondii alone. For cats infected with T. gondii, the responses of lymphocytes to T. gondii antigen were not affected by FIV infection; the responses to FIV antigen were negligible in all groups. Overall, this study indicates that FIV infection favors T. gondii proliferation. Also, the establishment of toxoplasmosis may enhance FIV-induced immunodeficiency and is likely to cause a more rapid disease progression than that from infection with FIV alone.
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PMID:Immunological changes in cats with concurrent Toxoplasma gondii and feline immunodeficiency virus infections. 134 3

Sulfated polysaccharides have been shown to inhibit human immunodeficiency virus (HIV) infection in vitro. Dextrin sulfate, fucoidan, and dextran sulfate fail to neutralize virions directly, but interact with target cells to inhibit virus entry. Ionic interactions of sulfated polyanions with oppositely charged cell surface components, including CD4, have been assumed to be the inhibitory mechanism. It is shown that the sulfated polysaccharides inhibit infection of both CD4+ and CD4- cell lines by HIV and also that they inhibit HTLV-1 and, to a lesser extent, the simian retrovirus, MPMV, which use receptors other than CD4. One binding site for radiolabeled fucoidan on the surface of human T cells is an 18 kD protein, but its significance is not yet clear.
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PMID:Investigations into the mechanism by which sulfated polysaccharides inhibit HIV infection in vitro. 134 67

Despite the occurrence of hypergammaglobulinemia in human immunodeficiency virus (HIV) infection, specific antibody production and in vitro B-cell differentiation responses are frequently impaired. In this study, we have examined the effects of HIV envelope glycoprotein gp120 on T-helper cell function for B cells. In the culture system used, B-cell functional responses were dependent on T-B-cell contact, since separation of T and B cells in double chambers by Transwell membranes rendered the B cells unresponsive in assays of antigen-induced B-cell proliferation and differentiation. Cytokines secreted by T cells were also essential, since anti-CD3 monoclonal antibody (mAb)-activated, paraformaldehyde-fixed T-cell clones failed to induce B-cell proliferation and differentiation. Pretreatment of the CD4+ antigen-specific T cells with gp120 was found to impair their ability to help autologous B cells, as determined by B-cell proliferation, polyclonal IgG secretion, and antigen-specific IgG secretion. The gp120-induced inhibition was specific in that it was blocked by soluble CD4. Furthermore, only fractionated small B cells (which are T-cell-dependent in their function) manifested impaired responses when cultured with gp120-treated T cells. Antigen-induced interleukin (IL)-2 and IL-4, but not IL-6, secretion were markedly reduced in gp120-treated T-cell clones. Addition of exogenous cytokines failed to compensate for defective helper function of gp120-treated T cells. The findings in this study indicate that gp120 impairs helper functions of CD4+ T cells by interfering with T-B-cell contact-dependent interaction; the inhibitory effects of soluble envelope proteins of HIV may contribute to the immunopathogenesis of the HIV-associated disease manifestations.
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PMID:Inhibition of normal B-cell function by human immunodeficiency virus envelope glycoprotein, gp120. 134 76

The Centers for Disease Control recommends that, because of a greatly increased susceptibility to pneumococcal infection, all persons infected with human immunodeficiency virus (HIV) receive pneumococcal vaccine. Using an ELISA specific for antibody to capsular polysaccharide, a postvaccination antibody was evaluated to five commonly infecting serotypes of Streptococcus pneumoniae. Thirty-nine HIV-infected persons with less than or equal to 500 CD4 cells exhibited significantly fewer responses than did healthy controls; overall, only 46 (24%) of 195 possible responses were positive compared with 45 (75%) of 60 in 12 HIV-infected subjects with greater than 500 CD4 cells and 92 (74%) of 125 in 25 healthy controls (P less than .001). Subjects with less than or equal to 500 CD4 cells responded to a mean of 1.1 antigens versus a mean of 3.8 and 3.7 in those with greater than 500 CD4 cells and controls, respectively (P less than .001). There were no differences between responses in those with less than 200 and those with 200-500 CD4 cells. Within groups stratified by CD4 cell counts, further stratification by clinical status did not reveal significant differences. Since asymptomatic HIV-infected persons with less than 500 CD4 cells show abnormal responses, pneumococcal vaccine should be given when HIV infection is first detected.
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PMID:Antibody to capsular polysaccharides of Streptococcus pneumoniae after vaccination of human immunodeficiency virus-infected subjects with 23-valent pneumococcal vaccine. 134 58

In vivo infection of monocytes/macrophages by the human immunodeficiency virus (HIV) has been investigated in many studies since these cells were suggested to provide a reservoir for the virus. In this study, we wanted to find out whether HIV provirus could be detected in circulating monocytes and whether it could be compared with the provirus found in T lymphocytes (T-Ly). Twenty-one seropositive subjects were studied. The amplification method (PCR) was used with three different primer pairs (in gag, env, and long terminal repeat regions of the viral genome) to detect the HIV-1 genome in monocytes and T-Ly separated by an immunomagnetic isolation technique. Of 21 monocyte samples, 13 (61.9%) were positive with at least one primer pair. Furthermore, the provirus harboured in 9 of those 13 monocyte-positive samples differed, with respect to pattern of primer response, from the provirus found in T-Ly. When comparing primer responses of monocytes and T-Ly, most of the differences were found to have occurred with the env primers (8 of 9 cases). Dilution experiments with the 8 E5 cell line revealed that 9 of 12 T-Ly contained 15-150 HIV DNA copies per 150,000 cells while 8 of 11 positive monocytes contained less than 15 copies. However, monocyte samples from two asymptomatic individuals and an AIDS patient showed high levels of HIV DNA, comparable to those obtained in T-Ly. Finally, it was also found that the monocyte-positive subjects were more immunosuppressed than the negative ones, as shown by the total CD4 count of both groups (means of 269 T4/mm3 and 573 T4/mm3, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HIV-1 in blood monocytes: frequency of detection of proviral DNA using PCR and comparison with the total CD4 count. 134 27

beta-Carotene is a nontoxic carotenoid with immunomodulating properties in animals and humans. Based on our observations in normal immunocompetent subjects, we studied the effects of this compound in 11 patients infected with the human immunodeficiency virus (HIV). Each subject received 60 mg of beta-carotene daily for 4 mo. Clinical and laboratory studies were obtained at baseline, every month while on treatment and for 2 mo after treatment. Increases in the percent of cells expressing Leu 11 (natural killer cells), Ia antigen and transferrin receptor (activated lymphocytes) were observed after 3 mo of treatment with beta-carotene and diminished thereafter. Major changes were not seen in total lymphocyte count or in the percent of cells expressing CD11, CD8 or CD4 antigens. No clinical toxicity was observed. These data suggest that beta-carotene can modulate certain immune markers in HIV-infected subjects. Further study of this compound in HIV infection may be warranted.
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PMID:A preliminary trial of beta-carotene in subjects infected with the human immunodeficiency virus. 134 16

The mechanisms of human immunodeficiency virus (HIV-1) entry into CD4+ cells and HIV-1 inactivation by sCD4 were studied by analyzing the kinetics of inhibition of viral infection by sCD4 and the kinetics of fusion of CD4+ cells with intact virions labeled with the lipid fluorophore octadecylrhodamine (R18). sCD4 inhibited HIV-1 infection much more effectively when preincubated with virus prior to interaction with CD4+ cells than when mixed simultaneously with virions and cells. The kinetics of inhibition of infection was much slower at 4 degrees and at low sCD4 concentrations than at 37 degrees and at high sCD4 concentrations. In the absence of sCD4, attachment of virus to cells leading to productive infection occurred within 10-30 min. Fusion of the virions with cells started after a 1-2 min lag time and was complete within 15 min. In high-density cell suspensions (5 x 10(7) cells/ml), even very high sCD4 concentrations (100 micrograms/ml) failed to block viral infection during simultaneous mixing of cells, sCD4 and HIV-1. We conclude that the kinetics of sCD4-virus interaction and the competition of sCD4 with the cell surface associated CD4 for the virus are crucial factors in the inhibition of HIV-1 infection by sCD4. These results provide insight into mechanisms of viral penetration into cells and should be considered when designing new approaches for AIDS therapy.
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PMID:Kinetics of HIV-1 interactions with sCD4 and CD4+ cells: implications for inhibition of virus infection and initial steps of virus entry into cells. 134 67


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