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)

A cross-sectional seroepidemiologic study was carried out between 1985 and 1990 in 1,567 heterosexual intravenous drug users who had been seen at the AIDS Regional Reference Center in Palermo, Italy, to evaluate the rate of human immunodeficiency virus type 1 (HIV-1) seroprevalence in this group and its long-term trend. Sixty serum samples collected from drug users in 1980 and 1983, before the founding of the Center (1985), were tested as well. Some demographic and behavioral risk factors were studied in a subgroup of intravenous drug users enrolled in 1985, 1987, and 1990 for their possible association with HIV-1. These factors were also studied in relation to hepatitis B virus infection, since both viruses share the same modes of spread. These drug users had a higher prevalence of markers for hepatitis B virus than of HIV-1 antibodies, and the prevalence rates in sera collected declined over time for both infections. The presence of both antibodies to HIV-1 and markers for hepatitis B virus was independently associated with the age of the drug user, the duration of drug use, and the year of serum collection. Antibodies to HIV-1 were observed more frequently in females than in males. No relation was found between education or employment status and the presence of HIV-1 antibodies or hepatitis B virus markers. Although new HIV-1 infections still occur, the decline in seroprevalence observed at the end of the 1980s might be related to modifications in social behavior among newer drug users, partial exhaustion of the susceptible population, and increasing risk awareness in more experienced users.
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PMID:The changing pattern of human immunodeficiency virus type 1 infection in intravenous drug users. Results of a six-year seroprevalence study in Palermo, Italy. 162 37

Young adult rats exposed to a 1 hr feeding schedule in activity-wheel cages daily, show immunological incompetence and stomach ulcer. This stress procedure is called "activity-stress (AS)". The present study examined the effects of neurotropin (NSP), which is an extract from rabbit skin tissues inflamed with vaccinia virus, on the immunosuppression and stomach ulcer induced by AS. The i.p. treated NSP showed a significant immunopotentiation effect (50 and 100 mg/kg), but did not significantly prevent the ulceration, although i.p. treated NSP decreased the incidence of ulcer. The p.o. treated NSP revealed both immunopotentiation (50 and 100 mg/kg) and antiulcerogenic effects (100 mg/kg). However, the i.p. treatment of NSP seems to prevent atrophy of the thymus and spleen, but did not improve hypertrophy of the adrenals induced by AS. The p.o. treated NSP improved atrophy of the spleen and hypertrophy of the adrenals, but did not improve atrophy of the thymus. Since immunodeficiency and ulcer-production by AS are considered to be phenomena appearing in the exhaustion stage of the organism, the present study suggests that NSP can heal immunological incompetence and stomach-ulcer induced by stress. In addition, the present study discussed the different pharmacological activities of NSP based on differences between administration routes.
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PMID:Effects of Neurotropin on immunodeficiency and ulcer-development of rats exposed to activity-stress. 344 16

Severe trauma, major surgery and burns (TSB) are often followed by infections, adult respiratory distress syndrome and multi-organ failure, complications which are thought to be the consequence of the post-TSB immunodeficiency syndrome. The most important data and hypotheses in this regard are summarized. After a TSB event large amounts of tissue debris, endotoxins and microorganisms have to be eliminated. Further important factors in TSB are stress reactions, malnutrition, loss and replacement of fluids and therapeutic measures. The elimination of unwanted elements is partly carried out by non-specific mechanisms such as opsonisation, chemotaxis and phagocytosis by granulocytes and cells of the macrophage/monocyte lineage, while specific reactions of humoral and cellular immunity also play a role. Severe TSB is thought to be associated with growing exhaustion of the unspecific defense system, leading to deficient specific immune reactions. Routinely measurable parameters only partly reflect the complex events after TSB: there is a decline in serum levels of fibronectin, immunoglobulins and some components of complement, in chemotaxis, phagocytosis and intracellular killing, and in circulating T3 and T4 lymphocytes as well as some lymphocyte functions. Some of these measurable parameters of defense mechanisms are statistically predictive for the occurrence of infections and other sequelae of TSB. Specific prophylactic and therapeutic measures can only be taken, if at least some of the complex events after TSB are better understood.
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PMID:[Post-traumatic/postoperative immune deficiency syndrome]. 355 99

Human immunodeficiency virus (HIV)-specific cytotoxic T lymphocytes (CTLs) are thought to play a major role in the immune response to HIV infection. The HIV-specific CTL response is much stronger than previously documented in an infectious disease, yet estimates of CTL frequency derived from limiting-dilution analysis (LDA) are relatively low and comparable to other viral infections. Here we show that individual CTL clones specific for peptides from HIV gag and pol gene products are present at high levels in the peripheral blood of three infected patients and that individual CTL clones may represent between 0.2% and 1% of T cells. Previous LDA in one donor had shown a frequency of CTL precursors of 1/8000, suggesting that LDA may underestimate CTL effector frequency. In some donors individual CTL clones persisted in vivo for at least 5 years. In contrast, in one patient there was a switch in CTL usage suggesting that different populations of CTLs can be recruited during infection. These data imply strong stimulation of CTLs, potentially leading some clones to exhaustion.
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PMID:Persistent high frequency of human immunodeficiency virus-specific cytotoxic T cells in peripheral blood of infected donors. 759 26

Progression to acquired immunodeficiency syndrome (AIDS) has been related to exhaustion of the regenerative capacity of the immune system resulting from high T cell turnover. Analysis of telomeric terminal restriction fragment (TRF) length, a marker for cellular replicative history, showed that CD8(+) T cell TRF length decreased but CD4(+) T cell TRF length was stable during the course of human immunodeficiency virus type-1 (HIV-1) infection, which was not explained by differential telomerase activity. This observation provides evidence that turnover in the course of HIV-1 infection can be increased considerably in CD8(+) T cells, but not in CD4(+) T cells. These results are compatible with CD4(+) T cell decline in HIV-1 infection caused by interference with cell renewal.
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PMID:T cell telomere length in HIV-1 infection: no evidence for increased CD4+ T cell turnover. 892 18

To address the possible role of replicative senescence in human immunodeficiency virus (HIV) infection, telomere length, telomerase activity, and in vitro replicative capacity were assessed in peripheral blood T cells from HIV+ and HIV- donors. Genetic and age-specific effects on these parameters were controlled by studying HIV-discordant pairs of monozygotic twins. Telomere terminal restriction fragment (TRF) lengths from CD4+ T cells of HIV+ donors were significantly greater than those from HIV- twins. In contrast, telomere lengths in CD8+ T cells from HIV+ donors were shorter than in HIV- donors. The in vitro replicative capacity of CD4+ cells from HIV+ donors was equivalent to that of HIV- donors in response to stimulation through T cell receptor CD3 and CD28. Little or no telomerase activity was detected in freshly isolated CD4+ or CD8+ lymphocytes from HIV+ or HIV- donors, but was induced by in vitro stimulation of both HIV+ and HIV- donor cells. These results suggest that HIV infection is associated with alterations in the population dynamics of both CD4+ and CD8+ T cells, but fail to provide evidence for clonal exhaustion or replicative senescence as a mechanism underlying the decline in CD4+ T cells of HIV-infected donors.
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PMID:Telomere length, telomerase activity, and replicative potential in HIV infection: analysis of CD4+ and CD8+ T cells from HIV-discordant monozygotic twins. 910 24

We examine simple mathematical models to investigate the circumstances under which the dynamics of cytotoxic T-lymphocyte (CTL) activation and differentiation may result in the loss of virus specific CD8+ cells, a process known as CTL exhaustion. We distinguish between two general classes of viruses: (i) viruses infecting cells that are not involved in the immune response; and (ii) viruses infecting antigen presenting cells (APCs) and helper cells. The models specify host and viral properties that lead to CTL exhaustion and indicate that this phenomenon is only likely to be observed with viruses infecting APCs and helper cells. Moreover, it is found that for such viruses, a high rate of replication and a low degree of cytopathogenicity promote the exhaustion of the CTL response. In addition, a high initial virus load and a low CD4+ cell count promote the occurrence of CTL exhaustion. These conclusions are discussed with reference to empirical data on lymphocytic choriomeningitis virus and on human immunodeficiency virus.
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PMID:Dynamics of cytotoxic T-lymphocyte exhaustion. 949 6

Burnout in Acquired Immune Deficiency Syndrome (AIDS) care nursing is well described in the literature from a hospital based perspective. No studies into the effects of AIDS care and burnout have been carried out within the community setting. A two-stage, mixed method study was carried out. In Stage one 30 Clinical Nurse Specialists in human immunodeficiency virus (HIV)/AIDS from the North of England completed the Maslach Burnout Inventory (MBI) and the AIDS Impact Scale. For Stage two five practitioners were selected randomly for semi-structured interview. Burnout morbidity was significant. Sixty-six per cent of informants scored as moderate or high burnout cases on the emotional Exhaustion and Personal Accomplishment subscales of the MBI. Only three per cent scored as cases on the depersonalization subscale. Links between the close involvement of practitioners with clients, death of clients, isolation, stigma and discrimination and the availability of support and supervision were identified as significant factors in AIDS care within this population that contributed to stress and burnout. Paradoxically, informants found the close relationships with clients, the autonomy of isolation and the exclusive nature of AIDS care positive aspects of their practice. The role of support and supervision in facilitating the continuance of a close empathic and therapeutic relationship and the prevention of an over-involved, isolated and stressful relationship is proposed as a way forward.
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PMID:Burnout and AIDS care-related factors in HIV community clinical nurse specialists in the North of England. 1021 92

In human immunodeficiency virus (HIV)-1 infection, highly increased T-cell turnover was proposed to cause exhaustion of lymphocyte production and consequently development of AIDS. Here, we investigated cell proliferation, as measured by expression of the Ki-67 nuclear antigen, in peripheral blood CD4(+) and CD8(+) lymphocyte subpopulations before and during highly active antiretroviral therapy (HAART). In untreated HIV-1 infection, both the percentage and number of Ki-67(+) CD4(+) and CD8(+) lymphocytes were significantly increased, compared with values obtained from healthy individuals. A more than 10-fold increase in the percentage of dividing naive CD4(+) T cells in the blood was found when the number of these cells were below 100 per microL. HAART induced an immediate decline in Ki-67 antigen expression, despite often very low CD4(+) T-cell numbers, arguing against increased proliferation being a homeostatic response. After approximately 24 weeks of HAART treatment, a transient increase in the number of proliferating cells was seen, but only in the CD4(+) CD27(+) memory pool. In the CD8(+) T-cell compartment, the number of dividing cells was elevated 20- to 25-fold. This increase was most notable in the CD27(+) CD 45RO(+) and CD27(-) CD45RO(+) memory CD8(+) T-cell pool, corresponding with the degree of expansion of these subsets. Reduction of plasma HIV-RNA load by HAART was accompanied by a decrease in numbers and percentages of dividing cells in all CD8(+) T-cell subsets. Taken together, our results indicate that peripheral T-cell proliferation is a consequence of generalized immune activation. (Blood. 2000;95:249-255)
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PMID:T-cell division in human immunodeficiency virus (HIV)-1 infection is mainly due to immune activation: a longitudinal analysis in patients before and during highly active antiretroviral therapy (HAART). 1060 9

Sooty mangabeys naturally infected with simian immunodeficiency virus (SIV) remain healthy though they harbor viral loads comparable to those in rhesus macaques that progress to AIDS. To assess the immunologic basis of disease resistance in mangabeys, we compared the effect of SIV infection on T-cell regeneration in both monkey species. Measurement of the proliferation marker Ki-67 by flow cytometry showed that mangabeys harbored proliferating T cells at a level of 3 to 4% in peripheral blood irrespective of their infection status. In contrast, rhesus macaques demonstrated a naturally high fraction of proliferating T cells (7%) that increased two- to threefold following SIV infection. Ki-67(+) T cells were predominantly CD45RA(-), indicating increased proliferation of memory cells in macaques. Quantitation of an episomal DNA product of T-cell receptor alpha rearrangement (termed alpha1 circle) showed that the concentration of recent thymic emigrants in blood decreased with age over a 2-log unit range in both monkey species, consistent with age-related thymic involution. SIV infection caused a limited decrease of alpha1 circle numbers in mangabeys as well as in macaques. Dilution of alpha1 circles by T-cell proliferation likely contributed to this decrease, since alpha1 circle numbers and Ki-67(+) fractions correlated negatively. These findings are compatible with immune exhaustion mediated by abnormal T-cell proliferation, rather than with early thymic failure, in SIV-infected macaques. Normal T-cell turnover in SIV-infected mangabeys provides an explanation for the long-term maintenance of a functional immune system in these hosts.
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PMID:Normal T-cell turnover in sooty mangabeys harboring active simian immunodeficiency virus infection. 1062 31


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