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)

Congenital deficiencies of developmental hormones, such as growth hormone and thyroxine, are responsible for the thymus-dependent immunodeficiency disease observed in dwarf mice. Such an immunodeficiency state is associated with early aging phenomena. This fact suggests that lymphoid cells and primarily T-derived cells are involved in the control of aging processes.
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PMID:Relation of lymphoid system and hormones to aging. 109 93

Growth hormone (somatotropin) is a potent anabolic protein currently being evaluated clinically in cachexia associated with malignancy and human immunodeficiency virus (HIV) disease. Growth hormone can also lead to enhancement of lectin-mediated cellular proliferation, macrophage activation, and cytokine induction, events linked to induction of latent HIV in vitro. We thus explored the ability of recombinant human growth hormone (rhGH) to affect viral replication in acute and chronic HIV infection, and to alter transcription at the HIV-1 long terminal repeat (LTR). A clone of promonocytic cells, chronically infected with HIV-1 and susceptible to viral induction by a variety of cytokines and protein kinase C activators, was unperturbed by rhGH used over broad concentrations (10 to 500 ng/mL) and time intervals. This unresponsiveness paralleled the lack of effect of rhGH on HIV-associated trans-activation in both monocytic and CD4+ T-cell lines. In contrast, rhGH enhanced viral replication in acutely infected peripheral blood mononuclear cells (PBMC) by twofold to 20-fold, albeit having no adverse effect on the antiviral efficacy of zidovudine (AZT). Augmentation of HIV growth correlated with stimulation of cellular DNA synthetic responses and an increase in tumor necrosis factor-alpha (TNF-alpha) secretion. These data are discussed in the context of ongoing clinical trials of rhGH in HIV-seropositive individuals with wasting syndromes.
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PMID:Effect of recombinant human growth hormone on acute and chronic human immunodeficiency virus infection in vitro. 173 91

Infection with human herpesvirus 6 (HHV-6) was found to up-regulate expression of human immunodeficiency virus and human T cell leukaemia virus type I (HTLV-I) long terminal repeat sequence (LTR), and herpes simplex virus type 1 (HSV-1) gD chloramphenicol acetyltransferase (CAT) constructs transfected into the T cell line, J. Jhan. Activation by HHV-6 was due to one or more viral proteins produced early in infection and, in the case of the HTLV-I LTR, was synergistic to induction mediated by the HTLV-I tax gene product. Neither the HTLV-I enhancer nor basal promoter elements of the HSV-1 gD gene were essential for activation and no increase in accumulated HTLV-I mRNA was observed due to HHV-6 infection. Induction by HHV-6 was found to be dependent on the reporter construct used, because the CAT gene and, to a lesser extent, the HSV-1 thymidine kinase gene were responsive to HHV-6 infection although no significant activation of growth hormone constructs was observed. Our results bear a strong resemblance to those obtained for the Epstein-Barr virus BMLF1 gene, indicating that the major HHV-6 trans-activator may be a homologue of this gene.
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PMID:Activation of gene expression by human herpesvirus 6 is reporter gene-dependent. 185 12

Sixteen human immunodeficiency virus type 1 (HIV-1)-seropositive children aged 5 to 12 years (nine girls and seven boys), born to HIV-1-infected mothers, were diagnosed between 1984 and 1987 in Kigali, Rwanda. They were compared with a group of age- and sex-matched HIV-1-seronegative children consecutively selected from the outpatient department. Two subjects were asymptomatic. Chronic cough was the most frequent symptom (seven of 16 patients). The most common signs were short stature (12 of 16 patients), low weight for age (seven of 16 patients), chronic parotitis (eight of 16 patients), persistent generalized lymphadenopathy (seven of 16 patients), and pulmonary tuberculosis (four of 16 patients). Lymphoid interstitial pneumonitis was diagnosed on radiologic grounds in five of 16 patients. Evidence of perivasculitis in the fundus was noted in three of 16 patients. Two children died during the study period (mean duration of follow-up, 40 months; range, 27 to 62 months); none of the other children had life-threatening infection or loss of developmental milestones. Immunologic assessment in the 16 children revealed high levels of IgG, decreased CD4+/CD8+ ratio, and skin test anergy. Endocrinologic investigations revealed normal thyroid function and normal basal human growth hormone levels but low basal insulinlike growth factor I levels (0.21 +/- 0.07 vs 0.44 +/- 0.20 U/mL for controls). In Kigali, perinatally HIV-1-infected children surviving beyond 5 years of age often present with moderate signs and symptoms, principally pulmonary involvement, chronic parotitis, and persistent generalized lymphadenopathy. Short stature is the major clinical manifestation in these patients and may be due, in part, to low growth hormone secretion rather than to malnutrition.
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PMID:Clinical and endocrinologic manifestations in perinatally human immunodeficiency virus type 1--Infected children aged 5 years or older. 195 Dec 15

The human immunodeficiency virus type 1 (HIV-1) tat protein functions at a much lower level in rodent cells than in human cells. This species-specific difference in trans activation appears to be due to the lack of a functional homolog of a human cofactor for tat in rodent cells. Using HIV-1 long terminal repeat-driven human growth hormone as a reporter plasmid, we found that the tat-mediated trans activation functions at a level 5- to 20-fold lower in rodent cells than in human cells. Stable rodent-human hybrid cells containing only human chromosome 12 support a dramatically higher degree of trans activation. Thus, human chromosome 12 encodes a species-specific HIV-1 tat cofactor which, at least partially, restores high levels of tat-mediated trans activation. Chromosome 6 also appears to provide an additional factor which enhances HIV-1 tat-mediated trans activation in murine cells.
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PMID:Human chromosome 12 encodes a species-specific factor which increases human immunodeficiency virus type 1 tat-mediated trans activation in rodent cells. 220 Aug 90

Vimentin is one member of the intermediate filament multigene family which exhibits both tissue- and developmental stage-specific expression. In vivo, vimentin is expressed in cells of mesenchymal origin. Previously, we identified both enhancer and promoter elements in the chicken vimentin gene which regulate gene expression in a positive manner. In this report, we have identified a 40-base-pair region at -568 base pairs between the proximal and distal enhancer elements which represses transcriptional activity. This silencer region can also repress the heterologous herpes simplex virus thymidine kinase promoter, which is comparable to the vimentin promoter. In addition, the element is able to function in a position- and orientation-independent manner, and the amount of repression is increased by multiple copies. Here we show by gel retardation assays and DNase I footprinting that this region binds a protein in nuclear extracts from HeLa cells. Southwestern (DNA-protein) blot analysis indicates this protein is approximately 95 kilodaltons in size. Moreover, protein distribution and activity mimic the expression pattern of vimentin during myogenesis, i.e., protein binding increases as vimentin gene expression decreases. The silencer region shares strong sequence similarity with 5'-flanking sequences found in both the human and hamster vimentin genes and with other characterized silencer elements, including the human immunodeficiency virus long terminal repeat, rat growth hormone, chicken lysozyme, and rat insulin genes. Thus, a negative element appears to bind a 95-kilodalton protein involved in regulating the tissue-specific expression of the chicken vimentin gene.
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PMID:A negative element involved in vimentin gene expression. 232 56

The BMLF1 region of the Epstein-Barr virus (EBV) genome and the immediate-early (IE) region of human cytomegalovirus (HCMV) both encode proteins which can trans-activate heterologous promoter/chloramphenicol acetyl transferase (CAT) constructs, including a human immunodeficiency virus type-1 promoter/CAT construct. We demonstrate here that this trans-activation by the EBV BMLF1 gene product, which we have previously shown to be largely post-transcriptional, is reporter gene dependent. In contrast, trans-activation by the HCMV-IE gene product(s), previously shown to be mediated at the RNA level, is seen regardless of whether CAT, human growth hormone, or beta-galactosidase is used as the reporter gene. Mutational analysis revealed no specific cis-acting sequences within the HIV-1 promoter which were required for trans-activation by the HCMV-IE gene product(s).
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PMID:Disparate effects of two herpesvirus [corrected] immediate-early gene trans-activators on the HIV-1 LTR. 255 54

The comparative study of the amino acid sequence of gp120 in human immunodeficiency virus (HIV) strains HTLV-III and ARV-2 and the amino end areas of the growth hormone receptors of human skin and the insulin receptors has been carried out, thus making it possible to predict the existence of two compact domains connected with an area of a peptide chain. This area is incapable of the formation of a compact globular structure due to a high content of the remnants of proline. The data obtained as the result of electron microscopic study in combination with image processing have confirmed the predicted three-dimensional structure of gp120. This study has also shown that the amino acid sequence of some regions in the domains of gp120 has a significant degree of homology with similarly located regions of the growth hormone and insulin receptors; in its turn, this amino acid sequence is homologous to the framework regions of the VH domain of immunoglobulin. Antibodies to this VH domain specifically react with recombinant HTLV-III antigen. On the basis of the data obtained in our experiments and from the analysis clinico-immunological information, we have come to the conclusion that AIDS is an autoimmune disease induced by HIV due to the structural homology of gp120 with highly important receptors of human cells.
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PMID:[The molecular bases of the pathogenesis of AIDS]. 255 69

A previously described patient with X-linked agammaglobulinemia and growth hormone deficiency developed an echovirus-associated meningoencephalitis and dermatomyositis-like syndrome while being treated with intramuscular gamma globulin and human growth hormone. Initiation of high-dose intravenous gamma globulin resulted in resolution of the clinical symptoms and the patient has remained asymptomatic over the past 55 months. Lymphocyte phenotype analysis at the time of presentation with echovirus infection revealed an increase in CD2+, CD16+, HNK-1+ lymphocytes, a decrease in CD4+ T cells as well as absence of B cells. This elevation in the LGL/NK phenotype resolved with clinical improvement. In addition, there was evidence of lymphocyte activation following the development of echovirus infection (increase in HLA-DR expression and elevated serum IL-2 receptor levels) which resolved with clinical improvement. A muscle biopsy obtained during the period of the dermatomyositis-like syndrome demonstrated a CD8+ lymphocytic infiltrate very similar to the observations in classical dermatomyositis. Taken together, these findings suggest that growth hormone therapy in this patient failed to alter the humoral immunodeficiency. In addition, serum IL-2 receptor levels and lymphocyte phenotyping may be useful adjuncts for monitoring echovirus disease in immunodeficient patients.
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PMID:Lymphocyte analysis in a patient with X-linked agammaglobulinemia and isolated growth hormone deficiency after development of echovirus dermatomyositis and meningoencephalitis. 275 12

Recently it has become evident that "second growth factor" of growth hormone (GH), such as somatomedins, has an effect on the proliferation and growth of tumor cells derived from nervous tissue. Effects of host-immunocompetence and the host-humoral states on the take incidence and proliferative activity of brain tumor cells were studied using two animal models: nude mouse and pituitary Snell dwarf mouse. Nude mouse is known to be immunodeficient. Pituitary Snell dwarf mouse is characterized by lack of circulating GH, TSH, prolactin, in addition to immunodeficiency. Cell line used in this experiment was C-6 cell of rat glioma cell. After intracranial implantation of C-6 glioma cells in the animals, the take incidence and growth rate of C-6 glioma cells were followed up and measured over a period of 2 months. Tissues of implants were studied immunohistochemically and biochemically. Regardless of cell line, successful take incidence in the different animal species was found to be greater in the descending order of nude mouse, dwarf mouse. This confirmed the role of immune status for the successful take of iso-, or heterologous tumor cells after implantation. We are now investigating the effect of exogenous GH on the growth rate of cells implanted in the dwarf mouse. This may clarify the effect of growth factors on proliferative activity of implanted tumor cells.
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PMID:[The correlation of host-immunocompetence and host-humoral states to the take incidence and proliferative activity of implantation C-6 glioma cells]. 276 6


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