Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper presents examination findings of 67 HIV-infected patients: 32 children aged 2.5 to 16 years and 35 adults aged 21 to 46 years. The proportion of patients with higher alpha-tumor necrosis factor and interleukin-1 beta increased with progression of the disease, the two parameters being higher in the children than in the adults. A correlation was found between the appearance of cytokines in the plasma and some clinical signs, such as fever, weight loss, anemia, neurological disorders. A parallel study of the patients' immunograms indicated significant correlations between the degree of impairments in the composition of lymphocyte subpopulations and the appearance of plasma cytokines.
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PMID:[Tumor necrosis factor-alpha and interleukin-1beta in the blood plasma of patients with HIV infection]. 128 18

We examined the mechanism of Tat-mediated trans activation through competition experiments employing Tat proteins of human immunodeficiency virus type 1 (HIV-1) and equine infectious anemia virus (EIAV). EIAV Tat, as well as chimeric EIAV/HIV-1 Tat proteins, inhibited HIV-1 Tat-mediated trans activation in a cell-type-dependent fashion. Furthermore, these proteins inhibited trans activation by Tat-bacteriophage R17 coat protein chimeras. Inhibition resulted from competition between activation domains of effectors and competitors for a limiting cellular cofactor. The context in which competitor activation domains were expressed contributed to the extent of inhibition. In transfected cells, EIAV Tat and all chimeric competitors were located primarily in the cytoplasm, whereas HIV-1 Tat was primarily located in the nucleus. These data are consistent with a model for trans activation in which the activation domain of Tat associates with and conveys a cellular factor to the transcription complex via the trans-acting-responsive element (TAR).
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PMID:Inhibition of human immunodeficiency virus type 1 Tat activity by coexpression of heterologous trans activators. 131 17

The nonstructural/regulatory genes of human immunodeficiency virus type 1 (HIV-1) and other lentiviruses are believed to play an important role in the replication and pathogenesis of these viruses. In HIV-1 and other lentiviruses, the vif (viral infectivity factor) open reading frame (ORF) (also termed sor or Q in some lentivirus genomes) is located in the central region, overlapping the 3' end of the pol ORF, but in a different reading frame. Among the lentiviruses, only equine infectious anemia virus lacks a vif ORF. The predicted Vif protein sequences from 38 lentiviruses were analyzed for the presence of global and local sequence similarity. The Vif proteins of closely related lentiviruses are highly conserved (HIV-1HXB2:HIV-1mn = 91% identity), while those of more distantly related lentirviruses have diverged significantly (HIV-1HXB2:simian immunodeficiency virusmax = 30% identity). A search for local sequence similarity revealed that a unifying feature of predicted lentivirus Vif proteins is the presence of at least one of two short, highly conserved sequence motifs, SL(I/V)X4YX9Y and SLQXLA. SLQXLA was present in 34 of 38 lentiviruses examined, while the remaining four lentiviruses had one (three viruses) or two (one virus) substitutions in this motif (of five total substitutions, three were conservative changes). The SL(I/V)X4YX9Y motif was found only in primate lentiviruses and in bovine immunodeficiency-like virus. Based on these findings, we suggest that the locus designation vif be used to denote all lentivirus ORFs previously called vif, Q, or sor.
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PMID:Conservation of amino-acid sequence motifs in lentivirus Vif proteins. 131 56

The drug zidovudine (AZT), a synthetic thymidine analogue, has been used in the treatment of acquired immunodeficiency syndrome (AIDS). Clinical use of zidovudine has induced haematopoietic toxicity manifested by anaemia, neutropenia, frequent thrombocytopenia, and overall bone-marrow suppression. The monovalent cation lithium has been shown to be an effective agent capable of modulating several aspects of haematopoiesis such as the induction of neutrophilia, thrombopoiesis, and protection against suppression of haematopoietic progenitor stem cells following exposure to anticancer drugs and/or radiation in the treatment of malignant disease. We here report the results of studies designed to evaluate the effectiveness of lithium in reversing and/or protecting against either murine or human bone marrow derived haematopoietic progenitors, i.e. (CFU-GM, CFU-Meg, and BFU-E) when co-cultured in the presence of zidovudine in vitro. Lithium chloride (LiCl) reversed zidovudine toxicity to either murine or human derived CFU-GM and CFU-Meg that was optimal at a concentration of 1 mM (P less than 0.05). However, the addition of lithium failed to influence zidovudine toxicity toward either murine or human BFU-E. In summary, these results support the scant clinical studies that have described the presence of neutrophilia and/or thrombopoiesis in zidovudine-treated AIDS patients receiving lithium. In addition, these data further confirm the need for more detailed evaluation of lithium as an adjuvant agent to reduce the haematopoietic toxicity associated with the use of antiviral therapy in HIV-infected patients.
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PMID:Effective modulation of the haematopoietic toxicity associated with zidovudine exposure to murine and human haematopoietic progenitor stem cells in vitro with lithium chloride. 131 88

The antiviral drug used in the treatment of acquired immunodeficiency syndrome, zidovudine, has proved effective in ameliorating the morbidity and mortality associated with human immunodeficiency virus infection. However, associated with zidovudine is the development of severe bone marrow toxicity manifested by anemia, neutropenia, and occasionally thrombocytopenia. We report the results of studies that demonstrate the ability of basic fibroblast growth factor (B-FGF) to reduce zidovudine toxicity to several classes of hematopoietic progenitors (granulocyte-macrophage, CFU-GM; megakaryocyte. CFU-Meg; and erythroid, BFU-E) from normal murine, human, and murine retrovirus-infected bone marrow cells when cocultured with zidovudine in vitro. Optimal response to B-FGF was observed at a dose concentration of 10 ng/ml. The specificity of B-FGF was demonstrated in the presence of protamine sulfate, an effective inhibitor of B-FGF mitogenic activity. In addition, synergistic activity of B-FGF on zidovudine-induced hematopoietic stem cell toxicity was observed in the presence of interleukin 1 (IL-1) (30 ng/ml). These studies demonstrate that B-FGF is capable of reducing the hematopoietic toxicity associated with zidovudine and that such an effect can be amplified in the presence of IL-1.
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PMID:In vitro modulation of the toxicity associated with the use of zidovudine on normal murine, human, and murine retrovirus-infected hematopoietic progenitor stem cells with basic fibroblast growth factor and synergistic activity with interleukin-1. 131 78

It was only in 1980 that the first human retrovirus, HTLV-1, was isolated. Since then, HTLV-2, HIV-1 and HIV-2 have been identified. All four viruses are transmitted with varying efficiency sexually, vertically from mother to infant, and through blood by transfusion or contamination. HTLV-1 is endemic in populations in south-west Japan, Taiwan, sub-Saharan Africa, the Caribbean, southern USA, central and south America, Australia, Papua New Guinea, Solomon Islands and western Asia. There is now epidemic spread amongst IVDUs in north and south America and southern Europe. HTLV-1 is the aetiological agent of adult T-cell leukaemia/lymphoma (ATL) and tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). Other associations which may be causative are with polymyositis, infective dermatitis, gastrointestinal malignant lymphoma and chronic lymphatic leukaemia. ATL appears to be due to malignant transformation of HTLV-1 infected cells, and TSP/HAM to chronic activation of these cells. The epidemiology of HTLV-2 is being separated only recently from HTLV-1 through the application of PCR. It has a low level of endemicity in populations of central Africa, and central and south America. It is being spread epidemically amongst IVDUs in north America and southern Europe. Its association with any pathology in man remains uncertain. HIV-1 is epidemic and spreading rapidly throughout the world. In areas where homosexual contact was the predominant mode of transmission, heterosexual spread is becoming increasingly important. The areas where heterosexual contact is the predominant mode of transmission include the worst affected populations in the world, for example sub-Saharan Africa and some of the Caribbean. There have been recent and explosive increases of HIV-1 seroprevalence in IVDUs and female prostitutes in Asia, especially Thailand and India. Of the diverse pathology following infection, only the haematological consequences are reviewed in detail: these include anaemia, leucopenia, thrombocytopenia, disorders of coagulation and lymphomas. HIV-2, compared to HIV-1, is less infectious and causes less immunosuppression with more slowly progressive disease. It is prevalent in west Africa, but is spreading, albeit slowly, far beyond.
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PMID:Human retroviruses. 132 49

The hematologic disorders that occur in HIV infected children are analysed by the authors, on the basis of some recent studies from current literature. There are emphasized the importance of the frequency of anemia, leukopenia and granulocytopenia. There are also stressed the pathogenic mechanisms of these disorders, their predictive significance and the rationale basis for therapeutics (actual and future treatment methods).
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PMID:[The hematological manifestations in human immunodeficiency virus (HIV) infection in children]. 133 73

Retroviruses of the nervous system cause HTLV-1-associated myelopathy and HIV-associated diseases. The treatment of HTLV-1 disease is essentially conservative; there is no effective drug treatment and therefore patients should be simply supported and reassured. If appropriate, other members of the family should be tested for HTLV-1 disease and counselled. The effects of HIV on the nervous system are much more complex. Therapy must take account of the diverse complications of HIV disease. Patients are probably best managed in specialized clinics which can cope with the different manifestations of the disease. Zidovudine (AZT) is the only effective anti-HIV drug that is licensed. It is indicated in complicated seroconversion disease and for any manifestation of HIV progression including AIDS dementia complex. Management of severe neurological disease depends critically on the ability to diagnose and treat CNS-specific opportunistic infections. Whether zidovudine is indicated for early asymptomatic disease when CD4 counts are below 500 microliters-1 is controversial. The main problems of zidovudine are reversible anaemia which results in about 30% of patients not tolerating long-term use, and the development of drug resistance which may be associated with clinical failure of the drug. Other, new and experimental drug treatments are discussed but none of them has as yet shown any convincing evidence of efficacy. Future improvements in treatment appear to depend on the development of effective multiple drug regimens (concurrently or sequentially) which will overcome the challenge of drug resistance.
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PMID:Therapeutic aspects of retroviral disease. 134 52

The signs that may arise after perinatal infection with human immunodeficiency virus type 1 (HIV-1) have been classified by the Centers for Disease Control, but the clinical usefulness of the classification system and the prognostic importance of each disease pattern have not been established. We sought to address these issues by analysing data from the Italian Register for HIV infection in children. We studied 1887 children born to HIV-1-seropositive mothers. 1045 were identified at birth and the others were registered later (median age 4.8 [range 0.4-72] months). HIV-1-associated signs developed in 433 (81.8%) of 529 seropositive infected children at a median age of 5 (0.03-84) months. These signs appeared significantly earlier in the 102 children who died of HIV-1-related illness than in those who are still alive (median 3 [0.03-55] vs 6 [0.03-84] months; p less than 0.001). The cumulative proportion surviving at age 9 years was 49.5% (95% confidence interval 27-65%) and the median survival time was 96.2 months. Separate analysis of the 112 seropositive infected children followed from birth and older than 15 months gave similar results. Hepatomegaly, splenomegaly, lymphadenopathy, parotitis, skin diseases, and recurrent respiratory tract infections formed the mildest disease pattern. Lymphoid interstitial pneumonitis and thrombocytopenia were signs of intermediate disease. By contrast, in multivariate analysis specific secondary infectious diseases, severe bacterial infections, progressive neurological disease, anaemia, and fever were significant and independent negative predictors of survival. Growth failure, persistent oral candidosis, hepatitis, and cardiopathy were associated in univariate analysis with significantly shorter survival. Our findings suggest that the outlook for children with perinatal HIV-1 infection is better than previously thought and that a new clinical staging system of single disease patterns is needed.
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PMID:Prognostic factors and survival in children with perinatal HIV-1 infection. The Italian Register for HIV Infections in Children. 134 67

Between October 1989-October 1990, health workers collected data on clinical presentation, receipt of transfusion, inhospital survival, and a capillary blood sample from 2433 12-year old children (median age=10 months) admitted to the pediatric ward of the Siaya District Hospital in rural western Kenya to determine when transfusion influences survival of children in the hospital. 29% of the children had severe anemia (Hb5 g/dl). Health workers administered blood transfusions to 20% of all children. Children with severe anemia were more likely to die than those who did not have severe anemia (18% vs. 8%; p.0001). Blood transfusion was associated with decreased mortality only if health workers administered blood transfusions to children with Hb3.9 g.dl during the day of admission (odds ratio [OR]=0.3) or the 1st day after admission (OR=0.37). Yet 41% of children needing a blood transfusion did not receive it until 2 days after admission. This exposed them to the risks of blood especially HIV infection when their chance of receiving any benefit was limited. Children with severe anemia and respiratory distress were also more likely to die than severely anemic children without respiratory distress (p.001). Children with Hb4.7 g/dl and respiratory distress who had received a blood transfusion had a lower mortality rate than those who did not receive a blood transfusion (OR=0.19). No association existed between children who showed no signs of respiratory distress regardless of Hb status and blood transfusion and mortality. Thus health workers at this hospital could improve child survival an reduce the frequency of blood transfusion by giving blood to children with severe anemia and clinical signs of respiratory distress during the day of or the 1st day after admission.
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PMID:Effect of blood transfusion on survival among children in a Kenyan hospital. 135 32


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