Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 5-year-old girl with a history of recurrent infection and anaemia has no measurable purine nucleoside phosphorylase (N.P.) activity in her red blood-cells. Her serum-immunoglobulin levels are normal, as are her antibody responses to thymus dependent and independent antigens. However, she has severe lymphopenia, pronounced depression of lymphocyte response to mitogenic and allogeneic cell stimuli, and greatly decreased T-cell rosette formation. Her parents are second cousins; their red cells contain less than half the normal level of N.P. activity. They also share an unusual N.P. isozyme pattern indicative of molecular hybridisation between catalytically active and inactive subunits, which strongly supports the assumption that they are heterozygous and their daughter is homozygous for a "silent" allele at the N.P. gene locus. Inherited deficiency of adenosine deaminase, an enzyme catalysing a reaction only one metabolic step away from that of N.P., is known to cause immunodeficiency. It is therefore very likely that this patient's lack of demonstrable N.P. activity is responsible for her syndrome.
 ...
PMID:Nucleoside-phosphorylase deficiency in a child with severely defective T-cell immunity and normal B-cell immunity. 4 76

The occurrence of T system immunodeficiency in an infant together with excessive production of IgM and, to a lesser degree, of IgG and IgA, is an unusual combination. A case is reported in which an unremitting lung infection with lymphadenopathy and hepatosplenomegaly developed in a previously healthy two-month-old infant. Leukocytosis with lymphocytosis, monocytosis and eosinophilia was rapidly followed by leukopenia and lymphocytepenia after a blood transfusion for anemia. There was a transient clinical remission, but on relapse 10 days later, quantitative and functional T cell deficiency was found together with increased IgG and IgA and with IgM values reaching 50 times greater than normal. Thymic humoral factor was successful in vitro in increasing the number of identifiable T cells (E rosetts) as well as T cell function (leukocyte migration inhibition factor production). However, the infant died suddenly, and at autopsy evidence of a generalized inflammatory reaction compatible with a viral infection was found. The thymus was small, hypoplastic and hypocellular. It is speculated that the T system deficiency may have been acquired following Epstein-Barr virus infection, and that T cell regulatory activity of immunoglobulin production was defective.
 ...
PMID:Immune deficiency of T system with possible T cell regulatory activity defect. 19 69

A potent inhibitor of cell proliferation was found in the urine of a patient with chronic renal failure. This substance included in "middle molecules" (MM) fraction, was obtained by chromatography. This factor was shown to inhibit noticeably the proliferation of various cells : lymphocytes stimulated by allogeneic cells, monolayer cell lines of normal or tumorous origin and leukemic cell lines derived from acute lymphoblastic leukemia. This effect was reversible and thus could not be related to a direct, rapid cytotoxic effect of MM. Such substances could play an important part in uremic symptoms, such as immunodeficiency, anemia, thrombopenia, gastrointestinal or skin manifestations.
 ...
PMID:A potent inhibitor of cell proliferation in "middle molecules" isolated from the urine of uremic patients. 54 28

Chronic lymphocytic leukemia (CLL) is the commonest type of leukemia seen in Western countries. It affects an older group of individuals than most other varieties of leukemia, and men more often than women, in a ratio of 2:1. The incidence of CLL is significantly increased in some families. In most instances, CLL is due to the overgrowth or accumulation of immunoglobulin producing B lymphocytes. Hypogammaglobulinemia is a common feature, and anomalous immunoglobulin components occur in 3 to 5% of patients. The early symptoms and signs of CLL include fatigue, reduced exercise tolerance, enlarged lymph nodes, and splenomegaly. Fever, weight loss, and impairment of bone marrow function, with anemia, bleeding and susceptibility to infection are characteristic of severe or advanced disease. In the great majority of patients, the disease can be controlled for 6 to 10 or more years with simple regimens using chlorambucil or cyclophosphamide, often in combination with prednisone. Radiotherapy and splenectomy are useful in some instances. The terminal phase of the disease is characterized by exacerbation or increasing severity of the leukemia and the development of opportunistic infections associated with immunodeficiency.
 ...
PMID:Chronic lymphocytic leukemia. 68 76

Cartilage-hair hypoplasia is an autosomal recessive osteo-chondrodysplasia which results in short stature, sparse hair and impaired cell-mediated immunity. In a study of 88 Finnish patients we found episodes of anaemia and/or macrocytosis during childhood in 86% of the patients. The reticulocyte index was always low in relation to anaemia. Bone marrow examination revealed decreased erythropoiesis in six of eight anaemic patients studied. Anaemia was most prevalent and severe during infancy. Spontaneous recovery occurred before adulthood in all patients except in three infants with fatal hypoplastic anaemia. Sixty-two percent of the patients had had lymphopenia and 24% neutropenia. Presence of anaemia significantly correlated to severity of immunodeficiency and growth failure and to presence of neutropenia. Disordered erythrogenesis is an integral feature of cartilage-hair hypoplasia and may, together with growth failure and immunodeficiency, reflect a generalized defect in cellular proliferation.
 ...
PMID:Anaemia and macrocytosis--unrecognized features in cartilage-hair hypoplasia. 129 Aug 47

The nonprimate lentiviruses feline immunodeficiency virus, equine infectious anemia virus, visna virus, and caprine encephalitis virus contain a gene segment in the polymerase gene that is lacking in the primate lentiviruses. A related sequence has been noted in other retroviruses, most notably the type D retroviruses. Computer searches have indicated a relatedness between this unique gene segment, termed proteaselike element and elements of both the aspartate proteinase and the dUTPase enzyme families. In this report, we show that members of both nonprimate lentiviruses and type D retroviruses possess dUTPase activity and present a formal demonstration that in feline immunodeficiency virus, the activity is encoded by the proteaselike element.
 ...
PMID:Distinct subsets of retroviruses encode dUTPase. 131 Jul 83

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).
 ...
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.
 ...
PMID:Conservation of amino-acid sequence motifs in lentivirus Vif proteins. 131 56

Feline immunodeficiency virus (FIV) has morphological, physical and biochemical characteristics similar to human immunodeficiency virus (HIV), the cause of AIDS in man. However, it is antigenically and genetically distinct from HIV; an antigenic relatedness with equine infectious anaemia virus has been demonstrated. FIV has been molecularly cloned and sequenced. Diagnostic tests are commercially available and attempts at preparing inactivated, subunit and molecularly engineered vaccines are being made in different laboratories. During FIV infection a transient primary illness can be recognized, with fever, neutropenia and lymphadenopathy. After a long period of clinical normalcy a secondary stage is distinguished with signs of an immunodeficiency-like syndrome. The incubation period for this stage can be as long as 5 years, during which gradual impairment of immune function develops. Many FIV-infected cats are presented for the first time showing vague signs of illness: recurrent fevers, emaciation, lack of appetite, lymphadenopathy, anaemia, leucopenia and behavioural changes. Later, the predominant clinical signs observed are chronic stomatitis/gingivitis, enteritis, upper respiratory tract infections, and infections of the skin. Neoplasias, neurological, immunological and haematological disorder are seen in a smaller proportion. The immunodeficiency-like syndrome is progressive over a period of months to years. Concomitant infection with feline leukaemia virus has been shown to accelerate the progression of disease. In vitro, phenotypic mixing between FIV and an endogenous feline oncovirus (RD114) has been demonstrated which leads to a broadening of the cell spectrum of the lentivirus. Bovine immunodeficiency virus (BIV) has been isolated only once, and all attempts to obtain additional isolates have failed; it has been recovered from the leucocytes of cattle with persistent lymphocytosis, lymphadenopathy, lesions in the central nervous system, progressive weakness and emaciation. As with the feline representative, BIV also was found to possess a lentivirus morphology and to encode a reverse transcriptase with Mg++ preference; it replicates and induces syncytia in a variety of embryonic bovine tissues in vitro. Antigenic analyses have demonstrated a conservation of epitopes between the major core protein of BIV and HIV. The original isolate has been molecularly cloned and sequenced. Besides the three large open reading frames (ORFs) comprising the gag, pol, and env genes common to all replication-competent retroviruses, five additional small ORFs were found. Numerous point mutations and deletions were found, mostly in the env-encoding ORF. These data suggest that, within a single virus isolate, BIV displays extensive genomic variation.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Animal immunodeficiency viruses. 133 43

The benefits of postexposure 3'-azido-3'-dideoxythymidine (AZT) prophylaxis following human immunodeficiency virus exposure are unknown. We describe a comprehensive assessment of pre- and postexposure AZT therapy in the feline leukemia virus (FeLV)-cat model for AIDS which included in vitro testing, an in vivo dose-response titration, a postexposure treatment study, plasma drug concentration determinations, and evaluation of the immune response to FeLV. In in vitro studies, AZT prevented FeLV infection of a feline T-lymphoid cell line, giving 50 and 90% inhibition concentrations of 4.6 and 11.1 mM, respectively. In all of the in vivo efficacy studies, AZT was administered by continuous subcutaneous infusion for 28 days. AZT toxicity was excessive at a dosage of 120 mg/kg of body weight per day, causing acute anemia, but AZT was tolerable at 60 mg/kg/day. In preexposure studies, AZT was efficacious in preventing chronic antigenemia at a dosage of > or = 15 mg/kg/day, at which plasma AZT concentrations averaged between 0.51 and 0.81 micrograms/ml (2.13 and 3.03 microM). As a postexposure treatment, at 60 mg/kg/day, AZT prevented chronic FeLV antigenemia when treatment was started up to 96 h post-virus inoculation (p.i.), but not when treatment was started at 192 h p.i. The 4-day period between 96 and 192 h p.i. appears to be critical for establishing chronic viremia. It is presumed that the increase in virus load between 4 and 8 days p.i. was able to overwhelm the immunologic functions responsible for containment of FeLV infection, even though AZT therapy effectively controlled viremia during the treatment period. The antibody response to FeLV varied depending on the time of AZT treatment initiation relative to virus challenge. When AZT treatment was started 48 h before or 8 h after FeLV challenge, antibodies to FeLV were not detected until after AZT treatment was discontinued at 28 days p.i. Following AZT treatment, however, antibody titers rapidly increased at a rate suggestive of a secondary immune response. When AZT treatment was initiate at later time points relative to virus challenge (24, 48, and 96 h p.i.), antibodies to FeLV became detectable during the treatment period. These results indicate that AZT treatment does not completely prevent FeLV infection, even when treatment begins before virus challenge, and that immune sensitization to FeLV proceeds during the prophylactic drug treatment period.
 ...
PMID:Pre- and postexposure chemoprophylaxis: evidence that 3'-azido-3'-dideoxythymidine inhibits feline leukemia virus disease by a drug-induced vaccine response. 133 45


1 2 3 4 5 6 7 8 9 10 Next >>