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)

The human immunodeficiency virus (HIV) was recently suggested to be involved in generating kidney lesions in HIV-associated nephropathy (HIVN). The possibility that antiretroviral agents can slow down the usually explosive evolution of HIVN to end-stage renal failure (ESRF) has not been studied in many of the series of cases published. The present work is a retrospective analysis of 11 patients with histologically proven HIVN, 6 of whom were treated with zidovudine. Seven patients (group 1) either required dialysis at the outset, when HIVN was diagnosed, or progressed very fast to ESRF within 15-45 days. Two patients of this group were treated with zidovudine, but it had no effect on kidney function. In the remaining 4 patients (group 2), HIVN progressed more slowly than in group 1. All 4 patients were treated with zidovudine at an earlier stage of the disease than ESRF. Only 1 deteriorated to ESRF in 9 months. The 3 others, who did not have ESRF, were followed up for 13, 10 and 32 months, respectively. Although this is a preliminary study, its results do suggest that zidovudine can slow down the evolution of HIVN to ESRF. They highlight the need to screen HIV-positive patients regularly for proteinuria, in order to detect HIVN by renal biopsies at an early stage of renal lesion formation.
Nephron 1992
PMID:Nephropathy associated with infection by human immunodeficiency virus: a report on 11 cases including 6 treated with zidovudine. 130 Apr 39

The Center for Devices and Radiological Health, in collaboration with the Department of Veterans Affairs Medical Center, Brooklyn, N.Y., conducted a multi-center, multi-institutional study of the seroprevalence of antibodies to the human immunodeficiency virus (HIV) among dialysis workers. Seven dialysis units and 112 dialysis workers participated in the study over a period of 2 years. Participation was limited to dialysis workers who, by questionnaire, denied non-occupational risk factors for HIV infection. The vast majority of the study participants were drawn from areas where the prevalence of HIV infection and AIDS cases are substantially greater than the national average. Study participants received the ELISA test for HIV antibodies. All 112 of the participants tested negative for HIV antibodies. These results are encouraging, as they failed to reveal unrecognized occupational transmission of HIV infection among dialysis workers.
Nephron 1992
PMID:Seroprevalence of antibodies to the human immunodeficiency virus in dialysis workers: results of a multi-center study. 130 Apr 40

Norepinephrine response to a cold pressor test was investigated in 95 homosexual men in a longitudinal study of human immunodeficiency virus (HIV) infection. The baseline data obtained from 76 HIV+ and 19 HIV- subjects are included in this report. After the insertion of a venicatheter and following a 30 min rest, subjects immersed one of their hands in ice water for 2 min, and serial blood samples were obtained for the determination of catecholamine levels. The results show that the norepinephrine response in HIV+ subjects compared to that of HIV- subjects was blunted. Examination of the responses using linear and quadratic orthogonal polynomials suggested that these differences between the two groups were primarily a function of their rate of increase in norepinephrine levels. It was observed also that in HIV+ subjects, norepinephrine level peaked earlier than that in HIV- subjects. The data suggest that autonomic dysfunction is present in the early stages of HIV infection.
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PMID:Norepinephrine response in early HIV infection. 185 90

Spontaneous lymphoblastoid cell lines (LCLs) were established from the peripheral blood of ten human immunodeficiency virus (HIV)-seropositive patients in order to investigate whether or not a progression of the cells toward a malignant state could be traced. The LCLs studied displayed no differences in their surface phenotype, karyotype, or tumorigenicity in nude mice when compared with a wide panel of control LCLs. However, four of the ten LCLs derived from HIV-seropositive patients formed colonies in agar with a cloning efficiency (0.1 to 0.9%) that was much lower than that of a control neoplastic B cell line (50%). Some sublines that were derived form the agar colonies expressed new activation markers (CD10 and Bac-1) but did not produce tumors in nude mice or display chromosomal abnormalities. These sublines might comprise cells that have progressed toward a more transformed state.
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PMID:Assessment of the potential malignancy of Epstein-Barr virus (EBV)-infected B cells in AIDS-related disorders. 216 68

Four Epstein-Barr virus-positive lymphoblastoid cell lines (LCL) were successfully infected in vitro with immunodeficiency virus type 1 (HIV-1) as demonstrated by reverse transcriptase activity and p24 HIV antigen in culture supernatants, positive cell staining for gag-encoded HIV proteins, presence of viral HIV genome by Southern blot analysis and ulstrastructural observations. In addition, both HIV-1-infected B cells and their supernatants efficiently transactivated the chloramphenicol acetyl transferase reporter gene which is under the control of the HIV-1 long terminal repeat. The LCL cells displayed long-term HIV-1 infection and production, but no cytopathic effects were observed. Cytofluorimetric analysis did not detect membrane CD4 presence in the LCL cells before and after HIV-1 infection; moreover, a minute amount of CD4 mRNA was observed only in one of the LCL. A monoclonal antibody specific for the viral binding site of the CD4 molecule delayed, but did not block, HIV-1 infection of the LCL cells. Following HIV-1 infection, changes in LCL phenotype were observed, consisting of a decrease in CD23- and CD39-positive cells, and a concomitant increase of cells with surface CD10 and Bac-1. Furthermore, HIV-1-infected LCL cells did not grow in tight clumps, as usually observed in uninfected LCL, but as disperse suspensions, and formed more agar colonies than control LCL. However, despite this apparent acquisition of a malignant-like phenotype, c-myc proto-oncogene rearrangement was not detected. The appearance of cells with new characteristics did not seem due to clone selection by HIV-1 infection, since all the LCL conserved their clonotypic pattern of IgH chain rearrangement. The acquisition of malignant-like features by HIV-infected B cells might be clinically significant in terms of the pathogenesis of non-Hodgkin's B cell lymphomas, which occur frequently in AIDS patients.
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PMID:Infection of Epstein-Barr virus-transformed lymphoblastoid B cells by the human immunodeficiency virus: evidence for a persistent and productive infection leading to B cell phenotypic changes. 217 Jan 47

We examined the influence of uremic serum on antigen receptor triggered T cell proliferation in dialysis patients with impaired immune function, i.e., 12 nonresponders to hepatitis B vaccination. The dialysis patients showed a monocyte dysfunction and an increased responsiveness to interleukin 2 (IL-2) according to our previous findings. In vitro the addition of IL-2 completely reconstituted the defect. Uremic serum inhibited monocyte-dependent T cell proliferation of patients and of healthy controls. Contrary, monocyte-independent steps of T cell proliferation were not impaired by uremic serum. When IL-2 was added to cultures, the T cell proliferation in the presence of uremic serum was even enhanced. We conclude that uremic immunodeficiency may be enhanced by soluble factors present in uremic serum which inhibit monocyte-dependent steps of T cell proliferation.
Nephron 1990
PMID:Uremic serum inhibits monocyte-dependent, but not interleukin-2-dependent steps of T cell proliferation. 224 71

Spontaneous lymphoblastoid cell lines (LCLs) were established from the peripheral blood of 10 human immunodeficiency virus (HIV)-seropositive patients in order to investigate whether or not progression of the cells towards a malignant state could be traced. The LCLs studied displayed no differences in their surface phenotype, karyotype, and tumorigenicity in nude mice as compared with a wide panel of control LCLs. Furthermore, no c-myc rearrangement could be detected in any of the LCLs. However, 4 of the 10 LCLs derived from HIV-seropositive patients formed colonies in agar with a cloning efficiency of 0.1-0.9%. This percentage was much lower than that of a control neoplastic B cell line (50%), but consistently higher than that observed for a battery of spontaneous LCLs. The cells of a number of sublines that were derived from the agar colonies expressed new activation markers (CD10 and Bac-1) but did not induce tumors in nude mice or display chromosomal abnormalities. These sublines might comprise cells that have progressed towards a more markedly transformed state.
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PMID:Studies on the oncogenic potential of Epstein-Barr-virus (EBV)-infected B cells in AIDS-related disorders. 255 27

Uremic patients are at high risk of hepatitis B virus (HBV) infection and, despite the availability and efficacy of hepatitis B vaccine, a high rate of non responders has been reported. Forty uremic patients undergoing maintenance hemodialysis who failed to produce any measurable anti-HBs antibody response after 4 administrations of 5 micrograms of Hevac B Pasteur vaccine were admitted to a randomized controlled clinical trial. Group A (14 patients) received 3 doses of 5 micrograms s.c. each of vaccine at monthly intervals and 12 doses of 50 mg s.c. of thymopentin on alternate days between the first and the second vaccination. Group B (11 patients) received 3 doses of 5 micrograms s.c. each of vaccine at monthly intervals. Group C (15 patients) received 3 doses of 10 micrograms s.c. each of vaccine at monthly intervals. Immunization rates were 86% in group A (on both 1-month and 6-month checks), 36% on the 1-month and 27% on the 6-month check in group B, 53% on the 1-month and 47% on the 6-month check in group C. Anti-HBs antibody titers were similar in group A and C but notably lower in group B. Thymopentin seems as useful therapeutical tool for non responder patients. As it promotes T cell maturation and responsiveness, which are impaired in uremia, it could play a major part in the management of uremic immunodeficiency.
Nephron 1988
PMID:Controlled trial of thymopentin in hemodialysis patients who fail to respond to hepatitis B vaccination. 306 61

An 11-year-old boy developed Kaposi's sarcoma and progressive T lymphocyte deficiency 5 years after cadaveric kidney transplantation for end-stage renal disease. He had received 17 individual red blood cell transfusions prior to and during transplantation in 1980. Human immunodeficiency virus (HIV) was cultured from blood in cerebrospinal fluid and HIV antibodies were detected with enzyme immunoassay and immunoblot techniques. The recipient of the donor's other kidney was well and HIV antibody-negative. The patient was treated with etoposide with excellent although transient regression of tumor. Allograft function has remained stable despite minimal immunosuppressive therapy and the need for high-dose anticonvulsant therapy. This case represents the first pediatric patient with acquired immune deficiency syndrome (AIDS) and Kaposi's sarcoma following kidney transplantation.
Nephron 1987
PMID:Human immunodeficiency virus-associated Kaposi's sarcoma in a pediatric renal transplant recipient. 330 30

Assays for suppressor cells were used to investigate the immunological status of uraemic patients (39) and transplant patients (66), and results were compared with those for normal controls (52). The functional assays were depletion of suppressor activity by preincubation (suppressor index) and the concanavalin-A-inducible suppressor assay and, in the uraemic patients, T gamma, T mu, and T0 cells were enumerated. The results of these assays were discordant, supporting previous suggestions that they measure different suppressor cell populations. The level of concanavalin-A-inducible suppressor cell activity was significantly below normal in both uraemic and transplant patients. The number of T mu cells in uraemia was significantly reduced. The findings do not support the possibility that suppressor cells are involved in the immunodeficiency of uraemia or the maintenance of renal transplants. Moreover, it could be suggested that uraemic toxaemia depresses both helper and suppressor modalities with the net effect being a 'pan-deficiency' of immune function.
Nephron 1982
PMID:Suppressor cells in stable dialysis and transplant patients. 621 27


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