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)

Two immunologically distinct glycoproteins, fractions C4 and C6, with a molecular weight of 28,000 and 28,500, respectively, estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, were isolated from seeds of Luffa cyclindrica using acetone precipitation, gel filtration on Sephadex G-75, and ion exchange chromatography on CM-Sepharose CL-6B. Fractions C4 and C6 correspond to luffin-a and luffin-b, respectively, according to the ion exchange chromatographic behavior and amino acid compositions. Fraction C6 and luffin-b were characterized by a lower content of threonine and a higher content of proline than fraction C4 and luffin-a. The 2 luffins, the protein from Luffa acutangula (luffaculin) and trichosanthin exhibited an overall similarity in amino acid composition. The proteins differed in the content of aspartic acid, threonine, proline, and alanine but were otherwise similar in amino acid composition. The ribosome inactivating proteins from Luffa cylindrica seeds also possessed abortifacient activity: they were capable of inducing mid term abortion in mice, inhibiting protein synthesis in a cell-free system, and suppressing thymidine uptake by human choriocarcinoma cells. The abortifacient activity of these proteins is possibly the result of their inhibitory effects on the biosynthetic activity of implanting embryos and endometrial cells. Trichosanthin inhibits the replication of human immunodeficiency virus (HIV) in acutely and chronically infected cells of lymphocyte and mononuclear phagocyte lineage with a potential in AIDS therapy. However, it is still unknown whether the proteins from Luffa cylindrica seeds also possess anti-HIV activity.
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PMID:Two proteins with ribosome-inactivating, cytotoxic and abortifacient activities from seeds of Luffa cylindrica roem (Cucurbitaceae). 150 59

Human choriocarcinoma cells of the JAR line, with no demonstrable surface CD4 receptor were infected with human immunodeficiency virus type 1 (HIV-1), strain RF. Primer-directed enzymatic DNA amplification (polymerase chain reaction, PCR) detected the presence of viral DNA when the cultures were investigated at day 5 post-infection (p.i.). The absence of cytopathic changes attributable to virus replication suggested silent infection of these malignant trophoblastic cells. Neither reverse transcriptase (RT) activity nor HIV-specific antigens were found in the culture nutrient medium during JAR cell propagation. However, when the HIV-carrier JAR cells were continuously cultured and the cocultivation was initiated with CEM-SS lymphoblastoid cells after two subsequent passages, rescue of infectious virus was observed.
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PMID:In vitro productive infection of human malignant trophoblastic cell line JAR with human immunodeficiency virus type 1 (HIV-1). 168 80

An in vitro model of placental infection by human immunodeficiency virus type 1 (HIV-1) was established using human choriocarcinoma-derived trophoblast lines exposed to free HIV-1 or HIV-1-infected lymphocytic and monocytic cells. Virus infectivity was evaluated by measuring both the levels of p24 HIV-1 antigen and reverse transcriptase activity either from indicator MT-4 lymphocytes after co-cultivation with infected trophoblasts or directly from trophoblast cultures. None of the tested trophoblast lines were permissive, in a detectable manner, to infection by cell-free virus. Furthermore, there were no signs of infection when trophoblasts were exposed to HIV-1-carrying ACH-2 and U1 cells with impaired adhesion capacity. However, the exposure to MOLT-4/IIIB lymphocytes or U937/YH5 monocytes that adhere to substrate cells resulted invariably in productive infection. The ultrastructure of the trophoblasts suggests endocytosis of HIV-1. It appears that the infection of the host cell results from the escape of virions from degradation in lysosomes. Alternatively, HIV-1 may enter by budding directly from the lymphocyte surface into the cytoplasm of trophoblasts. These results confirm previous studies and suggest that CD4-negative placental trophoblasts--the only foetal cells in direct contact with maternal blood--can be susceptible to HIV-1 infection.
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PMID:Human immunodeficiency virus type 1 infection of choriocarcinoma-derived trophoblasts. 810 49

A composite element that interacts with multiple nuclear receptors has been identified in the long terminal repeat (LTR) of the human immunodeficiency virus-1 (HIV-1). This element, designated nuclear receptor-responsive element (NRRE), spans the -356 to -320 LTR region and contains tightly clustered binding sites for the retinoid X receptor-alpha (RXR alpha) and for five nuclear receptors with unknown ligands, apolipoprotein AI regulatory protein-1 (ARP-1), v-erbA-related proteins-2 and -3 (EAR-2 and EAR-3), hepatocyte nuclear factor-4 (HNF-4), and nerve growth factor-inducible protein-B (NGFI-B). The NRRE also interacts with heterodimers formed between RXR alpha and either ARP-1, EAR-2, EAR-3, the retinoic acid receptor-alpha (RAR alpha), or the peroxisome proliferator-activated receptor (PPAR). Remarkably, nuclear receptor binding is conserved in the LTRs of recently evolved HIV-1 strains but it is absent in the oldest and most divergent viral isolates, raising the intriguing possibility that the NRRE has been evolved recently in the viral genome. Cotransfection experiments in human choriocarcinoma JEG-3 cells have shown that the HIV-1 LTR-driven transcription is activated by RXR alpha and RAR alpha in the presence of 9-cis- and all-trans-retinoic acid, by PPAR and RXR alpha in the presence of clofibric acid and 9-cis-retinoic acid, and by the "orphan" receptors HNF-4 and NGFI-B. These findings suggest that a complex network of nuclear receptor signaling pathways, that include 9-cis- and all-trans-retinoic acid, fatty acids, peroxisome proliferators, growth factors, membrane depolarization, and possibly other signals, converge onto the HIV-1 NRRE and may participate in modulation of viral gene expression.
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PMID:Convergence of multiple nuclear receptor signaling pathways onto the long terminal repeat of human immunodeficiency virus-1. 811 38

The acyclic nucleoside phosphonate 9-(2-phosphonylmethoxyethyl)adenine (PMEA) is a potent and selective antiretroviral agent which is currently evaluated in its oral prodrug form, bis(POM)PMEA (adefovir dipivoxil), in phase II and III clinical trials in human hepatitis B virus (HBV)- and human immunodeficiency virus (HIV)-infected individuals, respectively. We have now found that PMEA is also a potent inhibitor of growth of the highly aggressive choriocarcinoma tumor arising from rat choriocarcinoma RCHO cells grafted under the kidney capsule of syngeneic WKA/H rats. In untreated rats, massive invasive RCHO tumors, covering the whole surface of the kidney and resulting in a marked enlargement of the kidney, were observed at day 10 after tumor cell grafting. Daily treatment with PMEA at 25 mg/kg/day afforded a marked reduction in tumor size (i.e., smaller tumors and slight, if any, enlargement of the kidney). Increasing the PMEA dose to 50, 100 or 250 mg/kglday resulted in a gradual increase of the antitumor effect of the compound. At the highest dose tested, i.e., 250 mg/kg/day, PMEA completely suppressed tumor growth. The antitumor activity of PMEA persisted for at least 10 days after termination of drug treatment. In addition, delayed treatment with PMEA at a dose of 200 mg/kg/day, started at a time point where choriocarcinoma tumors had already developed, stopped further growth and even induced regression of the tumors. PMPA, a closely related structural analogue of PMEA, failed to inhibit choriocarcinoma tumor growth. This observation points to the specificity of PMEA as an antitumor agent. In view of our findings, the therapeutic potential of PMEA for the treatment of neoplastic diseases appears to merit further investigation.
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PMID:Potent antitumor activity of the acyclic nucleoside phosphonate 9-(2-phosphonylmethoxyethyl)adenine in choriocarcinoma-bearing rats. 959 Jan 39

The appropriate management of gynecological malignancies in human immunodeficiency virus (HIV)-infected patients is uncertain. Gestational trophoblastic disease is highly curable and occurs predominantly among young females. However, such patients are often immunocompromised and cytotoxic agents may further compromise immunity. This case report demonstrates the successful management of choriocarcinoma in a HIV-infected patient.
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PMID:Choriocarcinoma and human immunodeficiency virus (HIV) infection: a case report. 1152 Mar 76

A 26-year-old woman with choriocarcinoma and acquired immunodeficiency syndrome initially presented with hydatidiform mole and was treated with dilation and curettage. Because of persistent elevation of serum beta human chorionic gonadotropin, the patient was treated with combination chemotherapy with etoposide, methotrexate, actinomycin D, cyclophosphamide, and vincristine (EMACO) for high-risk gestational trophoblastic tumor. The patient s initial stage was IIc. The serum beta human chorionic gonadotropin level returned to normal. Fourteen months later, the gonadotropin level again increased. The patient was treated with uterine curettage followed by vaginal hysterectomy. Despite further chemotherapy (with methotrexate and leucovorin, then oral etoposide), she died following metastasis of the tumor to the brain. Only four other cases of human immunodeficiency virus (HIV) infection with choriocarcinoma have been reported. There is no evidence to date that gestational trophoblastic disease is more prevalent in patients with acquired immunodeficiency syndrome. HIV infection and other immunodeficiency states, however, can influence the course of treatment and outcome in these patients. The low CD4 count in HIV infection may lead to a poor outcome despite chemotherapy.
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PMID:Choriocarcinoma in a patient with human immunodeficiency virus: case presentation and review of the literature. 1241 28

The appropriate management of gynecological malignancies in association with human immunodeficiency virus (HIV) infection is not established. To date the reported literature on the subject consists mainly of case reports. Due to the increasing prevalence of HIV infection, especially in sub-Saharan countries, the chances of finding both conditions in the same patient has produced management and ethical dilemmas. This retrospective study describes the management of 12 HIV-infected patients and compares their outcome with 29 non HIV-infected patients. The mean age of the non HIV-infected patients was 30 years (range 16-56 years), while the mean age of the HIV-infected patients was 32 years (range 20-47 years). In terms of risk factors, there were 72% of non HIV-infected women in the high-risk category compared to 50% of HIV-infected women (P = 0.468). All patients who received treatment had CD4 counts greater than 200 cells/microl. Two HIV-infected women who did not receive any form of chemotherapy due to low CD4 counts (41 cells/microl and 84 cells/microl) demised of their disease. The majority of women (86% non HIV-infected & 90% HIV-infected) received lfewer than 10 cycles of chemotherapy to attain cure. Most side effects were minor. None of the HIV-infected patients who received chemotherapy demised of their disease. In total, irrespective of risk category, there were 38 patients (93%) who were cured of their disease by chemotherapy including 10 HIV-positive patients. All patients were alive and free of disease at their last follow-up visit. Although the numbers are small, it is proposed that HIV-infected patients with choriocarcinoma and a reasonable degree of CD4 counts (>200cells/microl) should receive standard therapy.
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PMID:Gestational trophoblastic syndrome and human immunodeficiency virus (HIV) infection: a retrospective analysis. 1467 27

The type-I ribosome-inactivating protein trichosanthin (TCS) has a broad spectrum of biological and pharmacological activities, including abortifacient, anti-tumor and anti-human-immunodeficiency-virus (anti-HIV). In this study, circular dichroism (CD) and capillary electrophoresis were used for the first time to study TCS and its two TCS mutants of Y55G TCS (tyrosine 55 converted to glycine) and FYY140-142GSA TCS (tripeptide phenylalanine-tyrosine-tyrosine 140-142 converted to glycine-serine-alanine). The results indicated that the substitution of amino acids changed the secondary structures and the hydrophobility of TCS. Moreover, both Y55G TCS and FYY140-142GSA TCS demonstrated attenuated cytotoxicity and reactive oxygen species (ROS) production in human choriocarcinoma cells (JAR cells) as compared to natural TCS and wild-type TCS. Our results demonstrated the cytotoxicity of TCS on JAR cells and TCS-induced production of ROS might be TCS-conformational related, suggesting that CD and capillary electrophoresis study might throw new insight into the anti-tumor and anti-HIV mechanism of TCS.
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PMID:Capillary electrophoresis and circular dichroism study of trichosanthin and its mutants. 1896 45

Gestational trophoblastic disease (GTD) encompasses a spectrum of conditions ranging from hydatidiform mole to choriocarcinoma. The management of GTD in association with human immunodeficiency virus (HIV) infection is complicated by the interaction between chemotherapy, antiretroviral therapy, and poor performance status due to HIV-related illnesses. This study describes the profile of mortality of women with GTD in the background of HIV infection. A total of 78 patients with GTD were reviewed retrospectively. There were 53 patients with invasive molar pregnancy and 23 patients with choriocarcinoma. The HIV seroprevalence was 31%. There were 15 deaths (19%). There were 8 HIV-infected (33%) and 7 HIV noninfected (13%) who demised. Of the 8 patients with CD4 counts less than 200 cells/microL, 7 patients demised. There were no mortalities among patients with CD4 counts more than 200 cells/microL. Of the 15 deaths, 5 HIV-infected patients and 5 HIV-noninfected patients received chemotherapy. There were 5 patients admitted in very poor general condition precluding the administration of chemotherapy. Among the 10 patients that received chemotherapy and demised, the causes of death included widespread disease, multiorgan failure, and toxicity due to chemotherapy. These findings highlight the poor outcomes of HIV-infected women with CD4 counts less than 200 cells/microL due to poor tolerance to chemotherapy or poor performance status precluding administration of chemotherapy.
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PMID:Profile of mortality among women with gestational trophoblastic disease infected with the human immunodeficiency virus (HIV): argument for a new poor prognostic factor. 1939 11


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