Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four rhesus monkeys (Macaca mulatta) were inoculated with a homogenate of a cutaneous lepromatous leprosy lesion from a mangabey monkey (Cercocebus atys). One died of B-cell lymphoma, and another died of an immunodeficiency syndrome. Cell suspensions prepared from the tumor and spleen of the monkey with lymphoma induced lymphoma or an immunodeficiency syndrome when inoculated into additional young rhesus monkeys. The immunodeficiency syndrome was similar to simian acquired immunodeficiency syndrome and consisted of opportunistic infections, lymphoid hyperplasia or atrophy, wasting, and syncytial cell formation. Mitogen responses and percentages of T4- and T8-positive lymphocytes were normal until the animals were moribund. Lymphoblastoid cell lines became established in vitro from tumor cell suspensions. These cells were infected with a herpesvirus related to Epstein-Barr virus. In addition, a retrovirus morphologically similar to human T-cell lymphotrophic virus type III (HTLV-III) and simian T-lymphotrophic virus type III (STLV-III) was isolated from one of the lymphoblastoid cell lines (LCL). Type D retroviruses could not be demonstrated in the monkeys in the transmission study; however, a retrovirus similar to that in the LCL was isolated from 4 animals by coculture of peripheral blood lymphocytes with the human cell line H9. These results suggest that this retrovirus, STLV-III/Delta, may be associated with the immunodeficiency syndrome in these macaques and may be of mangabey origin.
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PMID:Transmissible lymphoma and simian acquired immunodeficiency syndrome in rhesus monkeys. 301 95

Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus's life cycle and to restore immune competence in immunocompromised patients.
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PMID:Vaccine and antiviral strategies against infections caused by human immunodeficiency virus. 328 28

The aim of this study was to ascertain the extent to which secondary disease and mortality in fully allogeneic chimeras (C57BL leads to CBA) is caused (if at all) by a delayed graft-versus-host reaction. Adult CBA males were thymectomized, irradiated, and reconstituted with T-lymphocyte-depleted C57BL or CBA bone marrow cells (BMC), followed three weeks after irradiation by implantation under the kidney capsule of thymic lobes from C57BL or CBA fetal or adult donors. These mice were observed for the development of secondary disease for periods in excess of 250 days, and they were examined at 5 weeks or 4 months for T lymphocyte reactivity and tolerance to alloantigens, using the cell-mediated lympholysis assay (CML). The following results were obtained. First, removal of T lymphocytes with anti-Thy 1 antibody and complement from allogeneic bone marrow did not prevent wasting and eventual death, although it prolonged the lifespan of mice substantially. Second, T lymphocytes generated from bone marrow-derived precursor cells became tolerant of the histocompatibility antigens of the thymus donor strain but remained normally reactive to third-party antigens. Third, allogeneic radiation chimeras did not survive as well as animals reconstituted with syngeneic cells, even when they were demonstrably tolerant in CML. Fourth, C57BL BMC maturing in a CBA host equipped with a C57BL thymus graft did not become tolerant of host antigens, indicating that extra-thymic tolerance does not occur in fully allogeneic--as opposed to semiallogeneic--chimeras. It is argued that the function of B lymphocytes and/or accessory cells is impaired in fully allogeneic radiation chimeras, and that the mortality observed was directly related to the resulting immunodeficiency. The relevance of the results described in this paper to clinical bone marrow transplantation is discussed.
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PMID:Tolerance, immunocompetence, and secondary disease in fully allogeneic radiation chimeras. 634 42

A syndrome of acquired immunodeficiency within a group of outdoor-housed rhesus macaques (Macaca mulatta) with unusually high mortality has been identified at the California Primate Research Center. The cause of death for most of the affected animals included septicemia and/or chronic diarrhea with wasting, often complicated by other problems. In many cases, multiple or unusual infectious agents were isolated or recognized, including cytomegalovirus, Cryptosporidium spp., and Candida albicans. Septicemias due to usually innocuous agents such as Staphylococcus epidermidis and Alcaligenes faecalis were seen. Two animals developed cutaneous fibrosarcomas. Affected animals had generalized lymphadenopathy and splenomegaly, with depletion of T-cell populations, initially follicular hyperplasia followed by depletion, and absence of plasma cells. This spontaneous disease syndrome in nonhuman primates has similarities to acquired immune deficiency syndrome (AIDS) in humans, providing an animal model for the study of the complex factors modulating the immune system.
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PMID:The pathology of an epizootic of acquired immunodeficiency in rhesus macaques. 669 18

Human immunodeficiency virus (HIV-1) associated wasting is an increasingly common clinical manifestation of AIDS. The pathogenesis of wasting is multifactorial and includes reduced caloric intake as a major contributing mechanism. The perceptions of taste and smell play an important role in stimulating caloric intake and in optimizing nutrient absorption through cephalic phase reflexes. The purpose of this study was to evaluate the degree of losses in taste and smell function that occur in subjects infected with HIV. Taste and smell function was evaluated in 40 HIV infected individuals and 40 healthy control subjects matched for age, sex, race, smoking behavior, and number of years of education. Chemosensory tests administered to subjects included taste and smell detection thresholds, taste and smell memory tests, taste and smell discrimination tests, and taste and smell identification tasks. Significant differences were observed between experimental and control subjects in glutamic acid taste detection threshold (p < 0.001), quinine hydrochloride taste detection threshold (p < 0.001), menthol smell detection threshold (p < 0.001) and in the taste identification task (p = 0.006). Overall the results suggest abnormalities in the peripheral and central nervous systems, and subjective distortion of taste and smell. A significant correlation was not established between CDC classification of HIV infection and taste and smell function, although trends were observed suggesting worsening function with progression of HIV disease. These results document significant taste and smell losses in HIV infected subjects which may be of clinical significance in the development or progression of HIV associated wasting.
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PMID:Taste and smell losses in HIV infected patients. 756 32

In Zimbabwe, there are about 120,000 pregnancies involving women infected with human immunodeficiency virus (HIV) each year--a finding that has major implications for the practice of gynecology and obstetrics in the country. For financial, cultural, and psychological reasons, HIV screening is not provided routinely to pregnant women in Africa. About 28% of infants of HIV-positive mothers are infected in utero (20% during labor) and an additional 14% are infected by breast feeding. To minimize vertical transmission of HIV, obstetricians are urged to avoid blood transfusions during delivery, clamp the umbilical cord as early as possible, use rubber cap vacuum extractors that prevent head abrasions, modify cesarean section techniques to reduce contact with maternal blood, and wipe rather than suction blood from the newborn's face. After delivery, HIV-infected women are at increased risk of puerperal sepsis, massive condylomata acuminata, fever, wasting, and mortality. No guidelines have been developed for the feeding of infants of HIV-infected mothers since formula is prohibitively expensive. Most African couples resist HIV testing. However, in cases where one or both partners are known to be infected, condoms, long-acting injectable contraception, or sterilization should be considered.
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PMID:Practising obstetrics and gynaecology in areas with a high prevalence of HIV infection. 765 5

We conducted a study to identify predictors of the wasting syndrome among human immunodeficiency virus 1 (HIV-1)-seropositive injecting drug users. We enrolled 113 cases (defined as an unexplained loss of > 10% baseline weight) and 226 controls (defined as < 5% weight loss or any weight gain) from a HIV-1-seropositive cohort of injecting drug users (N = 630) into a nested case-control study. Crude predictors of wasting included: older age [odds ratio (OR) for a 1-year difference = 1.06], female gender (OR = 1.66), more years spent injecting drugs (OR for 1-year difference = 1.05), presence of diarrhea (OR = 3.78), lower percentage of CD4 T-lymphocytes (OR for 10-unit difference = 0.73), and higher log beta 2-microglobulin concentration (OR for 1 log difference = 11.3). After adjusting for CD4 cell level, beta 2-microglobulin concentration, diarrhea, gender, length and frequency of drug use, age, the presence of thrush, and education, independent predictors of weight loss in HIV-seropositive injecting drug users were female gender (OR = 2.23) and increasing age (OR for 1-year difference = 1.06). Frequency and duration of drug use were not strongly associated with the odds of developing wasting syndrome in this HIV-1-seropositive cohort. These data indicate that HIV wasting syndrome in injecting drug users is distinct from complications of drug use.
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PMID:Age, gender, and other predictors of the wasting syndrome among HIV-1-infected injecting drug users. 774 5

A nested case-control study of vitamin A deficiency and wasting as risk factors for mortality from AIDS and infections was done within a large prospective cohort of human immunodeficiency virus (HIV)-infected injection drug users (IDUs). Fifty adult subjects who died from AIDS and infections were matched with 235 controls who survived. Plasma vitamin A, weight, and body mass index were measured. Mean length of follow-up was 2.4 +/- 1.1 years. Vitamin A deficiency occurred in 50% and wasting occurred in 38% of patients in the last visit before death. CD4 cells count < 200/microL, wasting, and vitamin A deficiency were associated with mortality. There was a higher risk of death in HIV-infected subjects with vitamin A deficiency (odds ratio [OR], 4.6; 95% confidence interval [CI], 1.8-11.3) and wasting (OR, 8.8; 95% CI, 2.7-28.2). Vitamin A deficiency and wasting are common during HIV infection and are independent predictors of mortality in HIV-infected IDUs.
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PMID:Vitamin A deficiency and wasting as predictors of mortality in human immunodeficiency virus-infected injection drug users. 856 25

Microsporidia are obligate, intracellular, spore-forming protozoal parasites. Their host range is extensive and includes most invertebrates and all classes of vertebrates. Five microsporidial genera (Enterocytozoon, Encephalitozoon, Septata, Pleistophora, and Nosema) and unclassified microsporidia have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. The majority of microsporidial infections in persons infected with human immunodeficiency virus (HIV) are attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Four cases of microsporidial infection among persons not infected with HIV who had documented or presumed cellular immunodeficiency and four cases of corneal stroma infection due to microsporidia in immunocompetent patients have been described. Furthermore, the first case of traveler's diarrhea due to E. bieneusi in an immunocompetent and otherwise healthy patient is reported in this issue. The sources of human microsporidial infections and modes of transmission are unknown.
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PMID:Microsporidial infections in immunodeficient and immunocompetent patients. 781 72

Microsporidia are obligate intracellular spore-forming protozoal parasites belonging to the phylum Microspora. Their host range is extensive, including most invertebrates and all classes of vertebrates. More than 100 microsporidial genera and almost 1,000 species have now been identified. Five genera (Enterocytozoon spp., Encephalitozoon spp., Septata spp., Pleistophora sp., and Nosema spp.) and unclassified microsporidia (referred to by the collective term Microsporidium) have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. Among persons not infected with human immunodeficiency virus, ten cases of microsporidiosis have been documented. In human immunodeficiency virus-infected patients, on the other hand, over 400 cases of microsporidiosis have been identified, the majority attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Diagnosis of microsporidiosis currently depends on morphological demonstration of the organisms themselves. Initial detection of microsporidia by light microscopic examination of tissue sections and of more readily obtainable specimens such as stool, duodenal aspirates, urine, sputum, nasal discharge, bronchoalveolar lavage fluid, and conjunctival smears is now becoming routine practice. Definitive species identification is made by using the specific fluorescein-tagged antibody (immunofluorescence) technique or electron microscopy. Treatment options are limited, but symptomatic improvement of Enterocytozoon bieneusi infection may be achieved with the anthelmintic-antiprotozoal drug albendazole. Preliminary observations suggest that Septata intestinalis and Encephalitozoon infections may be cured with albendazole. Progress is being made with respect to in vitro propagation of microsporidia, which is crucial for developing antimicrosporidial drugs. Furthermore, molecular techniques are being developed for diagnostic purposes, taxonomic classification, and analysis of phylogenetic relationships of microsporidia.
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PMID:Human microsporidial infections. 783


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