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)

We have proposed that inappropriate induction of programmed cell death (PCD) or apoptosis, a physiological cell-suicide process, may play a role in the pathogenesis of AIDS. This model has been supported by several reports of abnormal levels of PCD in vitro in both CD4+ and CD8+ T cells from human immunodeficiency virus type 1 (HIV-1)-infected persons. To further assess the significance of such a process in AIDS pathogenesis, in vitro PCD was compared in HIV-1-infected persons and in various primate models that allow discrimination between pathogenic chronic lentiviral infection either in the same species, such as rhesus macaques infected with different simian immunodeficiency viruses (SIV), or in different species, such as SIV-infected African green monkeys and HIV-1-infected chimpanzees. Abnormal levels of PCD in CD4(+)-T-cell-depleted peripheral blood mononuclear cells (PBMC), containing the CD8+ T cells, were observed in both pathogenic and nonpathogenic models. However, abnormal levels of PCD in the CD8(+)-T-cell-depleted PBMC, containing the CD4+ T cells, was only observed in the two models leading to AIDS: HIV-1-infected persons and rhesus macaques infected with a pathogenic strain of SIV. This suggests that inappropriate T-cell PCD in HIV-1-infected persons involves two distinct processes: one, concerning CD4+ T cells, is closely related to AIDS pathogenesis; and the other, concerning CD8+ T cells, may be a consequence of immune stimulation with no direct link to AIDS pathogenesis.
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PMID:Programmed cell death and AIDS: significance of T-cell apoptosis in pathogenic and nonpathogenic primate lentiviral infections. 793 84

The purpose of this paper is to give an overview of the psychiatric aspects of acquired immunodeficiency syndrome (AIDS)/human immunodeficiency virus (HIV) infection and sexually transmitted disease (STD) under the following subheadings: AIDS-related complex, AIDS hypochondriasis, AIDS dementia complex, AIDS and increased risk of suicide, psychiatric aspects of STD, and implications for the management of patients. The psychiatric aspects of HIV infection and AIDS include problems of adjustment to a diagnosis with a stigma and the threat of death, reactive depression and potential risk of suicide, personality disorder, AIDS-related complex (ARC), and AIDS-related dementia. The paper gives an overview of clinical, neuropathological and psychopathological experience in other countries with relevant examples from Papua New Guinea if available. STDs are mentioned because HIV transmission in Papua New Guinea is mostly by heterosexual means. The paper concludes by emphasizing the psychiatric principles of management of HIV-infected/AIDS/STD patients, which include pharmacotherapy but are always based on supportive psychotherapy and counselling.
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PMID:Psychiatric aspects of acquired immunodeficiency syndrome (AIDS)/human immunodeficiency virus (HIV) infection and sexually transmitted disease (STD): an overview. 805 45

The purpose of this study was to assess the suicide rate in people infected with the human immunodeficiency virus (HIV) in the general hospital population. A retrospective study of 2,363 psychiatric consultations was done in 1989 and 1990 at an urban municipal teaching hospital in New York City. The sample included 2,363 patients admitted to adult general care from January 1, 1989, to December 31, 1990, for whom consultations were requested from the consultation-liaison psychiatry service. Suicidal behavior was the reason for consultation in 21.8% of HIV-positive persons and in 19.8% of persons with acquired immunodeficiency syndrome. It was the reason for consultation in only 13.9% of persons with unknown HIV serostatus. This difference is statistically significant. The authors conclude that HIV seropositivity may be a significant risk factor for suicide in the general hospital patient population.
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PMID:HIV seropositivity as a major risk factor for suicide in the general hospital. 808 88

One of the difficulties in understanding the complex pathology of human immunodeficiency virus (HIV) infection is to explain the progressive depletion of the CD4 helper T cell population and consequently the destruction of the immune system. Although cytopathic effects of HIV are observed in vitro, they cannot in vivo account for CD4 T cell depletion because relatively few cells are productively infected. Thus immunological mechanisms must be envisaged. We have found that peripheral blood lymphocytes (PBLs) from asymptomatic HIV-infected individuals are primed for a suicide process known as apoptosis or programmed cell death (PCD). DNA fragmentation characteristic of apoptosis was enhanced by stimulation of lymphocytes with ionomycin, a known inducer of apoptosis in suitably primed cells. Identification of the T cell subpopulations programmed for apoptosis indicated that both CD4+ and CD8+ cells died when cultured without stimulation or when polyclonally stimulated with ionomycin. Activation-induced cell death was also observed after stimulation with self-MHC class II-dependent superantigens, namely bacterial toxins from Staphylococcus (SEB), Streptococcus (ETA), and Myocoplasma (MAM) and under these conditions the CD4+ T cells were preferentially affected. To explore whether new macromolecular synthesis were required for apoptosis, various known inhibitors of apoptosis such as cycloheximide, cyclosporin A, Zn2+, or EGTA were tested. Activation-induced apoptosis was found sensitive to these inhibitors, indicating an active mechanism, but apoptosis observed in nonstimulated cultures was not, suggesting that these cells already contained the complete machinery for death. Prevention of apoptosis could be obtained in the presence of a mixture of cytokines and the minimal signal necessary for this prevention was IL-1 alpha and IL-2. Finally, a correlation between PCD and AIDS-pathogenesis was suggested by the comparison of lymphocytes from lentivirus-infected primates suceptible (SIV-infected macaques) and resistant (HIV-infected chimpanzees) to AIDS. Altogether our results suggest that, during HIV or SIV infection, PCD may contribute in vivo to the deletion of reactive T cells after antigenic stimulation.
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PMID:Programmed cell death in AIDS-related HIV and SIV infections. 810 39

The empowerment and affirmation of lesbian, bisexual, and gay students is long overdue. This article explores how human immunodeficiency virus and acquired immune deficiency syndrome (HIV/AIDS), substance abuse, violence and hate-related crimes, suicide, and heterosexism all adversely affect the physical and emotional health of nonheterosexual college students. College health services must expand their current scope and practice and assume a leadership role in combating all forms of oppression by actively incorporating and addressing the unique health issues and needs of the lesbian, bisexual, and gay population. This article provides a brief overview of the relevant healthcare issues for lesbians, bisexuals, and gays; examples of heterosexism in college health services; and recommendations for institutional and personal and professional change.
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PMID:Challenging heterosexism in college health service delivery. 820 Nov 34

It has been hypothesized that programmed cell death (PCD), an active cell suicide process occurring in place of necrosis, can be associated with the pathogenesis of acquired immunodeficiency syndrome (AIDS). The entry of human immunodeficiency virus (HIV) into competent cells is mediated by the CD4 molecule present on the surface of certain lymphocyte subpopulations as well as on some cultured cell lines, e.g. U937 myelomonocytic cells. The present paper focuses on some specific aspects of PCD induced by the cytokine tumor necrosis factor (TNF). The results obtained indicate that the exposure of U937 cells to cycloheximide facilitates TNF-mediated PCD via a short term cell death program and modifies the expression of CD4 surface molecules. This change in surface antigen expression, manifested by internalization of the CD4 molecule, occurs in cells in which apoptosis has been triggered, but not in cells undergoing necrosis. These results indicate that the progression of cell death could be associated with specific alterations of certain surface molecules and could have a role in the entry of HIV into cells.
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PMID:Down-modulation of CD4 antigen during programmed cell death in U937 cells. 826 57

From May 1985 to December 1992, a total of 5,931,032 serum samples from eight population groups were tested for antibody to human immunodeficiency virus type 1 (HIV). Mandatory testing is carried out for blood donors, military recruits, immigrants, and prisoners. The other population groups were tested anonymously with consent. A total of 407 samples were seropositive. Of those HIV carriers, 63 developed AIDS: 37 were homosexuals, 6 were hemophiliacs, 1 was an intravenous drug user, 15 were heterosexuals, and 4 had no known risk factors. Although the prevalence of HIV infection and AIDS in Taiwan has remained low, the increase since 1988 has been rapid. Before 1987, all of the 48 persons with HIV infection were homosexuals or hemophiliacs. Thereafter, the risk groups diversified, with the main group shifting from homosexuals to heterosexuals and the number of intravenous drug users surpassing the number of hemophiliacs. Among the 63 patients with AIDS, 59 were male and only 4 were female; 53 have died (3 committed suicide).
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PMID:AIDS in the Republic of China, 1992. 827 97

High proportions of U.S. high school students engage in behaviors that place them at increased risk for the leading causes of death and morbidity (e.g., motor-vehicle crashes and other unintentional injuries, homicide, suicide, heart disease, and cancer), unintended pregnancy, and infection with human immunodeficiency virus (HIV) and other sexually transmitted diseases. Because efforts to measure health-risk behaviors among adolescents throughout the United States have not included those who do not attend school, the prevalences of those behaviors are probably underestimated for the total adolescent population. To characterize more accurately the prevalence of selected health-risk behaviors among adolescents aged 12-19 years who do and do not attend school, CDC analyzed self-reported national data from the Youth Risk Behavior Survey (YRBS), conducted as part of the 1992 National Health Interview Survey (NHIS). This report summarizes the results of the analysis.
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PMID:Health risk behaviors among adolescents who do and do not attend school--United States, 1992. 830 60

Many applications of somatic gene therapy relate to the immune system. Several forms of inherited immunodeficiencies are candidates for treatment by gene transfer. Adenosine deaminase (ADA) deficiency causes a form of severe combined immunodeficiency. Stable gene transfer and expression of human ADA has now been obtained in hematopoietic stem cells of mice and, more recently, in large animals. The human ADA has also been introduced and expressed in the primitive human hematopoietic progenitor cells that initiate long-term bone marrow culture. Clinical trials of gene therapy for ADA deficiency have been initiated. The initial protocols were aimed at the correction of peripheral blood T lymphocytes, but recent strategies are attempting ADA gene transfer into peripheral blood or bone marrow stem cells. Other immunodeficiencies that may soon be amenable to somatic gene therapy include leukocyte adhesion deficiency and chronic granulomatous disease. Gene therapy may also be applied to the treatment of acquired disorders. In theory, the hematopoietic stem cells of a human immunodeficiency virus (HIV)-infected patient could be genetically modified and used to reconstitute an HIV-resistant hematopoietic system. Various strategies are currently being investigated to achieve this "intracellular immunization" against HIV. These include the transfer of genes encoding recombinant soluble CD4 molecules, suicide genes under the control of HIV-inducible promoter, and anti-HIV ribozymes. Gene transfer could also be used in the treatment of cancer to increase the immune response of the host, to activate prodrugs specifically in tumors, or to protect normal tissues against the toxicities of conventional treatment. Recent progress in all of these applications of gene therapy is reviewed here.
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PMID:Gene therapy of the immune system. 847 64

Free peptide has been found to inhibit cytotoxic T lymphocyte (CTL) activity, and veto cells bearing peptide-major histocompatibility complex (MHC) complexes have been found to inactivate CTL, but the two phenomena have not been connected. Here we show that a common mechanism may apply to both. CD8+ CTL lines or clones specific for a determinant of the human immunodeficiency virus (HIV) 1 IIIB envelope protein gp160, P18IIIB, are inhibited by as little as 10 min exposure to the minimal 10-mer peptide, I-10, within P18IIIB, free in solution, in contrast to peptide already bound to antigen-presenting cells (APC), which does not inhibit. Several lines of evidence suggest that the peptide must be processed and presented by H-2Dd on the CTL itself to the specific T cell receptor (TCR) to be inhibitory. The inhibition was not killing, in that CTL did not kill 51Cr-labeled sister CTL in the presence of free peptide, and in mixing experiments with CTL lines of different specificities restricted by the same MHC molecule, Dd, the presence of free peptide recognized by one CTL line did not inhibit the activity of the other CTL line that could present the peptide. Also, partial recovery of activity could be elicited by restimulation with cell-bound peptide, supporting the conclusion that neither fratricide nor suicide (apoptosis) was involved. The classic veto phenomenon was ruled out by failure of peptide-bearing CTL to inactivate others. Using pairs of CTL lines of differing specificity but similar MHC restriction, each pulsed with the peptide for which the other is specific, we showed that the minimal requirement is simultaneous engagement of the TCR and class I MHC molecules of the same cell. This could occur in single cells or pairs of cells presenting peptide to each other. Thus, mechanistically, the inhibition is analogous to veto, and might be called self-veto. As a clue to a possible mechanism, we found that free I-10 peptide induced apparent downregulation of expression of specific TCR as well as interleukin 2 receptor, CD69, lymphocyte function-associated antigen 1, and CD8. This self-veto effect also has implications for in vivo immunization and mechanisms of viral escape from CTL immunity.
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PMID:Inactivation of human immunodeficiency virus (HIV)-1 envelope-specific CD8+ cytotoxic T lymphocytes by free antigenic peptide: a self-veto mechanism? 864 92


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