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)

Opportunistic infections are frequent in AIDS patients, particularly in the last phase of the disease, when they occur both singly and in combination with other conditions (for example KAPOSI's sarcoma). These opportunistic infections are the cause of death in over 90% of cases. Their incidence ist proof of cellular immunodeficiency. Based on our observations (17 cases at the two institutes since 1984) we present and discuss the histopathological changes of some important opportunistic infections (notably Pneumocystis carinii pneumonia, Mycobacteriosis (MAI), Cryptosporidium Cytomegalovirus and Toxoplasmosis gondii infection).
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PMID:[Histopathologic changes in several opportunistic infections in AIDS]. 281 71

The 3'-fluoro-and 3'-azido-substituted derivatives of 2',3'-dideoxythymidine (ddThd), 2',3'-dideoxyuridine (ddUrd), 2',3'-dideoxy-5-ethyluridine (ddEtUrd) and 2',3'-dideoxycytidine (ddCyd) have been synthesized and evaluated for their anti-retrovirus activity [against human immunodeficiency virus (HIV) and murine Moloney sarcoma virus (MSV)]. Based on their 50% effective doses the most potent inhibitors of HIV replication in human MT4 lymphocytes were: FddThd (0.001 microM), AzddThd (0.004 microM), FddUrd (0.04 microM) and AzddUrd (0.36 microM). Their selectivity indexes were 197, 5000, 500 and 677, respectively. In contrast, none of the 3'-substituted ddEtUrd derivatives had a marked antiviral effect. The 2',3'-dideoxynucleoside analogues showed poor, if any, substrate affinity for (bacterial) dThd phosphorylase. AzddThd and FddThd inhibited human dThd kinase to a much greater extent (Ki/Km: 0.66 and 3.4, respectively) than did AzddUrd or FddUrd (Ki/Km: 71 and 171, respectively). The Ki/Km values of FddCyd and AzddCyd for human dCyd kinase were about 60. Although phosphorylation is a prerequisite for the anti-retrovirus activity of the 2',3'-dideoxynucleoside derivatives, there is no close correlation between the anti-retrovirus potency of the 3'-fluoro- and 3'-azido-substituted ddUrd, ddThd, ddEtUrd and ddCyd derivatives and their affinity for dThd kinase or dCyd kinase.
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PMID:Anti-retrovirus activity of 3'-fluoro- and 3'-azido-substituted pyrimidine 2',3'-dideoxynucleoside analogues. 284 80

A study of the structure-activity relationship of a series of newly synthesized phosphonylmethoxyalkyl purine and pyrimidine derivatives revealed that several adenine derivatives substituted at the N9 position by a 2-phosphonylmethoxyethyl (PME) group inhibited human immunodeficiency virus (HIV)-induced cytopathogenicity and HIV antigen expression in vitro at concentrations significantly below the toxicity threshold for the host cells. In terms of anti-HIV potency in MT-4 cells, the PME 2,6-diaminopurine derivative (50% effective dose [ED50], 1 microM) ranked first, followed by the PME adenine derivative (ED50, 2 microM [MT-4]) and the PME 2-monoaminopurine derivative (ED50, 45 microM). Antiretroviral activity was also demonstrated in ATH8 and H9 cells, which were de novo infected with HIV, and extended to C3H mouse fibroblasts infected with Moloney murine sarcoma virus. Unlike 2',3'-dideoxyadenosine, these compounds were not found to be degraded by deaminases derived from bovine intestine.
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PMID:Phosphonylmethoxyethyl purine derivatives, a new class of anti-human immunodeficiency virus agents. 284 36

9-(2-Phosphonylmethoxyethyl)adenine (PMEA) is a potent and selective inhibitor of the replication of human immunodeficiency virus (HIV) in vitro in human T-lymphocyte MT-4, H9, and ATH8 cells. PMEA also inhibits Moloney murine sarcoma virus (Mo-MSV)-induced transformation of murine C3H embryo fibroblasts. Moreover, PMEA causes a dose-dependent suppression of tumor formation and associated mortality in mice inoculated with Mo-MSV. At a dose of 50 or 20 mg/kg per day PMEA effected a 90-100% protection of the mice against Mo-MSV-induced tumor formation and mortality. Even with a PMEA dose as low as 1 to 5 mg/kg per day, tumor formation was significantly delayed and the survival rate was significantly enhanced. In parallel experiments, azidothymidine exhibited a comparable inhibitory effect on Mo-MSV-induced tumor formation and associated death only at a 25-fold higher dose than PMEA. Because PMEA has stronger in vivo antiretrovirus potency and selectivity than azidothymidine and various other compounds currently being subjected to clinical trials, PMEA studies should be pursued to assess the potential of this compound in the treatment of acquired immunodeficiency syndrome (AIDS) and other retrovirus infections in humans.
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PMID:Marked in vivo antiretrovirus activity of 9-(2-phosphonylmethoxyethyl)adenine, a selective anti-human immunodeficiency virus agent. 291 79

The current rate of progression of persistent generalized lymphadenopathy to acquired immunodeficiency syndrome (AIDS) was tested in a cohort of 105 homosexual men in London, UK. 5 patients were lost to follow-up, and the remaining 100 were seen every 3 months. All tested positive for the human immunodeficiency virus antibody. Previous clinical observations had shown oral candida; anemia; leucopenia; thrombocytopenia; enthrocyte sedimentation rate 15 mm in the 1st hour to be possible predictors of AIDS. 5 of the 13 patients who developed AIDS during a mean follow-up period of 22 months (range 12-32) developed Pneumocystis carinii; 5 Karposi's sarcoma; 1 both; 1 P carinii and cryptosporidiosis; and 1 cryptococcal meningitis. A life table technic calculation showed that over 3 years the probability of patients with persistent generalized lymphadenopathy progressing to AIDS was 20.9%. Of the clinical features examined, those most likely to indicate progression to AIDS were Oral candida (relative risk (RR)=12); Lymphopenia (RR=7); Erythrocyte sedimentation rate 15mm (RR=7); and anemia (RR=6). There were figures for median time before AIDS onset and the range of variation of these median times for these symptoms, e.g. oral candida, 8 months median; range of 1-24 months. Similar prospective studies performed in the US are reviewed. It is determined that a clinical examination and hematological measurements are useful in determining progression risk.
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PMID:From persistent generalised lymphadenopathy to AIDS: who will progress? 310 80

We have constructed two related types of multi-cloning mammalian expression vectors. The first, pMPSVEH/HE, carries the promoter of the myeloproliferative sarcoma virus (MPSV). This promoter was found to be stronger than both the SV40 early and the trans-activated human immunodeficiency virus promoters in many cell lines including human and rodent fibroblastoid, lymphoid or myeloid cells. The other, pBEH/HE, carries the simian virus 40 (SV40) early promoter and origin of replication. This offers the possibility of encapsidation in SV40 pseudovirions and subsequent gene transfer into, e.g., hemopoietic cells, via infection. The usefulness of the expression systems was tested with a number of genes and cell lines.
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PMID:Vectors for efficient expression in mammalian fibroblastoid, myeloid and lymphoid cells via transfection or infection. 322 Feb 55

The acquired immunodeficiency syndrome AIDS is caused by the retrovirus HIV. About 20% develop after the inoculation of the virus an acute clinical picture resembling infectious mononucleosis. Several weeks to months after the infection antibodies can be demonstrated in the serum. Lateron a lymphadenopathy syndrome or AIDS related complex may develop. Most of the patients with LAS or ARC will progress to the full blown picture of AIDS. This is defined as immunodeficiency complicated by Kaposi-sarcoma or central nervous system malignance lymphoma or opportunistic infections. The most common infections are due to certain parasites, c. e. pneumocystis carinii, toxoplasma gondii and cryptosporidia. Fungi, bacteria and viruses can also cause opportunistic infections.
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PMID:[Clinical manifestations of acquired immunologic deficiency syndrome (AIDS)]. 347 26

Primary central nervous system lymphoma constitutes one of the criteria for the acquired immune deficiency syndrome (AIDS), yet a paucity of information is currently available regarding the clinical, immunologic, or pathologic features of these patients. Six homosexual men presenting with primary central nervous system lymphoma were evaluated. Five of these patients presented with altered mental status. All lymphomas were intracranial. B cell immunoblastic sarcoma was found in five. Immune phenotyping studies performed in five patients revealed monoclonal lambda light chain in three, whereas one expressed only IgG heavy chain, and one demonstrated another B cell (LN-1) surface antigen. Hypodense, contrast-enhancing lesions were apparent on computed axial tomographic scanning of the brain, in sharp contrast to isodense or hyperdense lesions reported in primary central nervous system lymphomas without underlying immunodeficiency. Immunologic abnormalities in these patients were similar to those in AIDS presenting as Kaposi's sarcoma or with opportunistic infections. In spite of therapeutic interventions, survival was short, and only one patient is currently alive.
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PMID:Primary central nervous system lymphoma in homosexual men. Clinical, immunologic, and pathologic features. 387 74

Tissues from patients thought to have Epstein-Barr virus (EBV)-induced lymphoproliferative diseases were probed for EBV genomes using 2 independent hybridization techniques. Tissues from six patients with the X-linked lymphoproliferative syndrome, all five renal allograft recipients with immunoblastic sarcoma, and eight patients with diverse types of immunodeficiency and lymphoproliferative diseases such as fatal infectious mononucleosis or malignant lymphoma associated with antecedent immunodeficiency contained significant numbers of EBV genome equivalents per cell. The use of 2 hybridization probes is recommended to confirm the presence of EBV genomes. The finding of significant numbers of EBV genomes in tissues from patients with immunodeficiency suggests that EBV is the etiological agent of the associated lymphoproliferative diseases.
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PMID:Documentation of Epstein-Barr virus infection in immunodeficient patients with life-threatening lymphoproliferative diseases by Epstein-Barr virus complementary RNA/DNA and viral DNA/DNA hybridization. 627 68

A fatal disseminated polyclonal malignant lymphoproliferative disorder of B-cells (immunoblastic sarcoma) developed shortly after a second thymic epithelial peritoneal implant in a 5-yr-old girl with combined immunodeficiency. The immunodeficiency was characterized by low T-cell numbers and function, very low levels of thymic hormone, dysgammaglobulinemia, and an inability to mount a primary antibody or cell-mediated response to new antigens. At necropsy, the thymus fulfilled morphological criteria for thymic dysplasia. Epstein-Barr virus (EBV) antigen and DNA were identified in neoplastic infiltrates in the lymph nodes and thymus by immunofluorescence for the EBV nuclear antigen and by EBV-specific complementary RNA/DNA hybridization. No antibodies to nuclear antigen, early antigen, or viral capsid antigen of EBV were identified in the serum. The concurrence of these events suggests that the thymic epithelial implant itself may have been instrumental in the pathogenesis of this neoplasm. It is proposed that the thymus may have provided factors which indirectly potentiated the proliferation of EBV-infected B-cells, possibly by induction of nonspecific T-helper cells and perhaps through other thymic humoral factors. It is suggested that some forms of immunoblastic sarcoma, even when polyclonal, and especially those which arise in immunocompromised hosts, may, in some instances, represent an opportunistic form of EBV-induced B-cell neoplasia.
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PMID:Epstein-Barr virus in a malignant lymphoproliferative disorder of B-cells occurring after thymic epithelial transplantation for combined immunodeficiency. 627 69


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