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)

Dementia is a common process in which there is gradual decrease in mental function due to disease of either cortical or subcortical structures. The numerous causes of dementia can be divided into those in which dementia is the primary manifestation, as in Alzheimer's disease, or secondary to chronic disease, neoplasms, endocrine and metabolic disorders and chronic infections. The dementia in AIDS is usually part of the syndrome of acquired immunodeficiency and may be its first manifestation.
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PMID:[AIDS-related dementia]. 784 51

In natural history studies of chronic disease, it is of interest to understand the evolution of key variables that measure aspects of disease progression. This is particularly true for immunological variables among persons infected with the human immunodeficiency virus (HIV). The natural time scale for such studies is time since infection. Most data available for analysis, however, arise from prevalent cohorts, where the date of infection is unknown for most or all individuals. As a result, standard curve fitting algorithms are not immediately applicable. Here we propose two methods to circumvent this difficulty. The first uses repeated measurement data to provide information not only on the level of the variable of interest, but also on its rate of change, and is based on the principal curves algorithm of Hastie and Stuetzle. The second uses an external estimate of the expected time since infection. Both methods use locally-weighted linear smoothers, and are applied to data from a prevalent cohort of HIV-infected homosexual men, giving estimates of the average pattern of CD4 lymphocyte decline. These methods apply to natural history studies that use data from prevalent cohorts where the time of disease origin is uncertain, provided availability of certain information from external sources.
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PMID:Estimating patterns of CD4 lymphocyte decline using data from a prevalent cohort of HIV infected individuals. 791 70

Visna-maedi virus is a lentivirus that causes a chronic disease in sheep affecting, among other organs, the lungs. Interstitial pneumonitis is similar to that in man associated with the infection by the human immunodeficiency virus type-1. We have compared the pathological features of lungs of sheep naturally infected with visna-maedi virus with the results obtained from bronchoalveolar lavage and virus isolation. Semi-quantitative grading of the lesions was performed on 147 sheep lungs obtained from the slaughterhouse. Seventy-seven were macroscopically and histologically normal, 39 had typical lesions of interstitial lung disease (maedi), and 13 had minor lesions of the same type. Eighteen of the affected lungs were heavily infested with parasites. Of these parasite-infected lungs, 9 showed typical maedi lesions and 4 showed minor lesions; parasite infection had no obvious effect on the development of maedi. In keeping with pathological findings, bronchoalveolar lavage disclosed an alveolitis process in the maedi lungs with increased macrophage, lymphocyte and neutrophil numbers. Cytopathic virus was detected from alveolar macrophage coculture with fibroblasts more often from maedi lungs (10/12) than from normal lungs (9/39). Electron microscopy of bronchoalveolar lavage cocultures revealed typical lentiviral particles. Animals with minor lesions may be at an early stage of the disease.
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PMID:Lentivirus-induced interstitial lung disease: pulmonary pathology in sheep naturally infected by the visna-maedi virus. 795 50

A chronic viral infection can occur when the host immune system fails to detect the viruses. Mouse hepatitis virus type 3 (MHV3) seems to be an excellent model for the study of the relationship between viral-induced immunodeficiency and the development of chronic disease. Animals that survive acute hepatitis develop a chronic disease characterized by viral persistency in various organs, including the brain, spleen, and thymus, and they eventually die within the next 3 mo postinfection (p.i.). To verify whether T and B cell immunodeficiency occurs either in the acute or chronic phase of the disease, the percentage and absolute number of splenic T and B lymphocytes, thymic T, or bone marrow B-lineage cell subpopulations were recorded at various times p.i. in pathogenic L2-MHV3-infected and nonpathogenic YAC-MHV3-infected (C57BL/6 x A/J) F1 mice. Splenic T and B cells were depleted as early as 48 h p.i., and maintained at low levels for up to 3 mo until death of mice. Such depletions resulted from thymic depletion in all T cell subpopulations, and in B (cytoplasmic micro-chain+ and surface micro-chain+) lymphocytes only in the bone marrow of pathogenic L2-MHV3-infected mice. In vitro studies of purified thymic stromal cells have produced a nonproductive L2-MHV3 replication with a low viral transmission to complexed thymocytes. However, pre-B and B cells have supported a productive viral replication, generating abnormal forms, which leads to cell lysis. These results are discussed in relation to viral persistency in the brain and lymphoid cells, which results from a chronic impairment of cellular and humoral immune mechanisms that are involved in the viral elimination process.
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PMID:Impaired T and B cell subpopulations involved in a chronic disease induced by mouse hepatitis virus type 3. 802 59

Immune mechanisms that may control Cryptosporidium parvum infection remain unknown. The role of T cell-mediated immunity is suggested by the chronic disease observed in AIDS patients and in athymic or CD4+ T cell-depleted mice. The role of specific antibodies is also unclear. This study sought to determine serum and secretory antibodies to C. parvum in patients infected with human immunodeficiency virus type 1 (HIV-1) with or without chronic cryptosporidiosis. C. parvum-specific antibodies and specific secretory antibodies were determined by ELISA in saliva and sera from 50 HIV-1-infected patients, 27 healthy adults, and 21 healthy children. Despite lower CD4+ lymphocyte counts, patients with chronic cryptosporidiosis had increased levels of C. parvum-specific antibodies in saliva and serum and higher specific secretory antibody levels in saliva than did controls. Persistence of protracted diarrhea despite high levels of both serum and secretory antibodies suggests that specific secretory antibodies are not sufficient to control this protozoan parasite infection of intestinal mucosa.
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PMID:Secretory IgA antibodies to Cryptosporidium parvum in AIDS patients with chronic cryptosporidiosis. 815 56

Equine infectious anemia virus (EIAV) is a lentivirus that causes a chronic disease of horses characterized by cyclic episodes of fever, anemia, and viremia. Although the genome and promoter of EIAV are much less complex than those of its relatives the primate immunodeficiency viruses, the cellular proteins that activate and regulate transcription of EIAV have not yet been identified. In this report, we show by electrophoretic mobility shift assays and DNase I footprinting that the EIAV promoter contains multiple binding sites for ubiquitous, cell type-specific, and inducible cellular proteins. Functional analysis by transient transfection of canine osteosarcoma (D17) and human epithelial carcinoma (HeLa) cells with EIAV promoters containing deletions or individually mutated DNA-binding sites demonstrated that these DNA-binding elements cooperatively regulate transcriptional activity. A methylated DNA-binding site (MDBP; also designated EF-C or EP) acts as either a positive or negative regulator of promoter activity, depending on the cell type or condition. Two PEA2 elements, an AP-1 site, and an ets/PEA3 motif confer a positive effect on promoter activity. The EIAV promoter is shown to be activated by treatment of HeLa cells with phorbol myristate acetate (PMA). DNA-binding activities were induced in PMA-treated HeLa cells and formed complexes on oligonucleotides that contain the EIAV AP-1 and ets/PEA3 elements. Functional analysis of mutated promoters indicated that the ets/PEA3 motif was the principal mediator of PMA activation.
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PMID:Physical and functional characterization of transcriptional control elements in the equine infectious anemia virus promoter. 838 28

An increasing focus on the human immunodeficiency virus (HIV) is important given the role of health psychology in preventing further spread of the epidemic and in maintaining quality of life in the estimated 1,500,000 Americans who are now infected. HIV presents health psychology with challenges reflecting 5 trends in medicine that have broad implications for the future, which extend beyond HIV: (a) the early identification of people who are at risk for disease, (b) the rising expectations for successful behavior change programs, (c) the growing populations of those who are coping with chronic disease, (d) the increasing shift to include community and public health perspectives, and (e) the emerging need to address health problems on a global scale.
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PMID:Health psychology in the 21st century: acquired immunodeficiency syndrome as a harbinger of things to come. 840 98

While the incidence of the human immunodeficiency virus (HIV) infection has leveled off somewhat in homosexual men, infection in women, children and adolescents is rising. Unless effective preventive measures are introduced, the number of pediatric patients with HIV and related illnesses will continue to increase. Animal models play a key role in the understanding of the pathogenesis and in the establishment of therapeutic approaches of infectious diseases. Ovine lentivirus (OvLV) comprises a subgenus of the lentivirus genus in the family Retroviridae, that shares genotypic, phenotypic and pathogenic features with HIV. Infection of sheep with OvLV results in a progressive chronic disease characterized by cachexia and chronic active inflammation in the lungs, lymph nodes, joints, mammary gland and the central nervous system. Pulmonary lesions in OvLV-affected sheep consist of lymphoid interstitial pneumonia (LIP) and lyphocytic alveolitis. Similarly, these pulmonary lesions also occur in up to 40% of HIV-infected children and in some adults with AIDS. Neonatal lambs experimentally inoculated intratracheally with OvLV develop LIP in 5 to 6 months, thus shortening by several years the natural incubation period and resembling the shorter incubation period observed in children with HIV-associated LIP. However, unlike HIV, OvLV does not infect CD4+T lymphocytes; OvLV only infects and replicates in macrophages. Recent studies indicate that macrophage tropic HIV plays an important role in disease progression. Similarities between HIV and OvLV argue for the use of ovine lentivirus infection as a model to advance in the understanding of some of the aspects of HIV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ovine lentivirus infection: an animal model for pediatric HIV infection? 855 28

Infection in humans with the lentivirus HIV-1 typically results in the development of a chronic disease state characterized by the slow decline of CD4+ lymphocytes, the development of immunosuppression, and the development of opportunistic infections, ultimately leading to death. Although the average course of disease runs approximately 10 years, shorter and longer progression times have been noted. These alterations are presumed to be, at least partially, a factor of viral variation. The simian immunodeficiency viruses (SIVs) are the nonhuman primate counterparts to HIV. Several of these isolates, including SIV from sooty mangabey monkeys, induce a remarkably similar disease in Asian macaques. Recently, variants of SIV from sooty mangabey monkeys and SIV from African green monkeys have been described, which are increasingly more pathogenic. As in HIV-1 infections, this is probably due to genetic variation. On the basis of these findings, atypical viruses with tremendous pathogenic potential can arise from apathogenic or moderately pathogenic viruses.
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PMID:Simian immunodeficiency virus variants: threat of new lentiviruses. 857 84

A chronic viral infection can occur when the host fails to mount an effective immune response to clear the virus. Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relationship between viral-induced immunodeficiency and chronic disease development. (C57BL/6 x A/J)F1 mice surviving acute hepatitis develop a chronic disease characterized by T- and B-cell immunodeficiencies, viral persistence in various organs including the brain, spleen and thymus, and death within 3 months postinfection (p.i.). We have reported that T- or B-cell deficiencies, observed in MHV3 chronically infected (C57BL/6 x A/J)F1 mice, can be partially or totally thwarted by adoptive transfer of CD4+, CD8+ and/or B cells, at 15 days p.i. in mice surviving the acute phase of the disease. Adoptive transfer of syngeneic CD4+ and/or CD8+ allowed a partial restoration of the T-cell deficiencies, as characterized by thymic atrophy, decrease in splenic T cells, and in all thymocyte subpopulations. B-cell immunodeficiency, as defined by a decrease in splenic B cells, as well as in the bone marrow pre-B- and B-cell compartments, and the occurrence of abnormally larger forms of bone marrow pre-B and B cells, were partially thwarted by B-cell treatment only. Splenic B cells and the bone marrow B-cell compartment, respectively, returned partially or totally to normal values, whereas the pre-B-cell compartment remained depleted in infected mice treated with B cells. Levels of all immunoglobulin classes returned to normal values in MHV3 chronically infected mice when treated with CD4+ in combination with CD8+ cells. All T- and/or B-cell treatments, however, were sufficient to thwart the process of the chronic disease, and favoured the survival of mice for up to 6 months p.i.
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PMID:Effect of adoptive transfer of CD4, CD8 and B cells on recovery from MHV3-induced immunodeficiencies. 869 Apr 54


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