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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection by human immunodeficiency virus type 1 (HIV-1) is associated with cellular activation and expression of the interleukin-2 (IL-2) receptor. A genetically engineered fusion toxin, DAB486 IL-2, that contains the enzymatic site and translocation domain of diphtheria toxin and the receptor binding domain of IL-2 specifically kills cells that express high-affinity IL-2 receptors. This toxin selectively eliminated the HIV-1-infected cells from mixed cultures of infected and uninfected cells and inhibited production of viral proteins and infectious virus. Thus, cellular activation antigens present a target for early antiviral intervention.
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PMID:Selective elimination of HIV-1-infected cells with an interleukin-2 receptor-specific cytotoxin. 190 28

Infection by the human immunodeficiency virus (HIV) leads to progressive destruction of the CD4+ subset of T lymphocytes, resulting in immunodeficiency and AIDS. The selectivity of CD4+ cell destruction is due to the specific binding of gp120, the external envelope glycoprotein of HIV, to CD4, initiating viral entry. Binding of gp120 to CD4 on the cell surface may also lead to CD4+ cell depletion by inappropriate immune targeting, and may interfere with CD4+ cell function and ontogeny by disrupting CD4-mediated cell signaling. The CD4-gp120 interaction is thus an obvious target for AIDS therapeutics.
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PMID:The CD4-gp120 interaction and AIDS pathogenesis. 191 Jun 91

Disorders of immunoglobulin synthesis are of great interest to rheumatologists. At the diagnostic level, such disorders not uncommonly mimic commoner rheumatic diseases, so it is important that the diagnostic possibility of immunodeficiency be kept in mind. Infections often complicate immunodeficiency and may present in an atypical manner. From the theoretical standpoint, the interactions between infectious agents and patients with impaired immunity suggest ways in which the same or similar agents could be responsible for arthritis of unknown etiology. Furthermore, many immunodeficiency disorders predispose to autoimmunity; establishing the mechanism of this association may offer good insights into the factors that trigger autoimmune disorders in patients with seemingly normal immune competence.
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PMID:Infectious arthritis in primary disorders of immunoglobulin synthesis. 191 Oct 59

Infection with the human immunodeficiency virus (HIV) and the development of the acquired immunodeficiency syndrome (AIDS) is a long-term process in many individuals. The progression of HIV disease is beginning to demonstrate many commonalities with other chronic diseases. Although research has not yet shown clear-out evidence that diet can make a difference in the course of disease in HIV-infected clients, nutrition should be viewed as an important component of holistic care for HIV-infected clients because: 1) wasting and symptoms of malnutrition are common problems associated with these clients; and 2) nutrition has proven to be a beneficial component of care in other chronic conditions. This paper uses the model developed by Winett, King and Altman (1989) to review nutritional support in HIV infection from a multilevel perspective ranging from personal psychology to institutional/societal controls. The author concludes that there is a potential benefit from integrating nutritional assessment, diagnosis and education into the holistic care of HIV-infected clients at the personal, interpersonal, organizational and societal levels.
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PMID:Nutritional support in HIV infection: a multilevel analysis. 191 56

Infection of macaques by the simian immunodeficiency virus (SIV), like HIV infection in humans, results in a variable time course to clinical disease. Developmental studies of macaques have shown that psychosocial disruption, including social separations, can result in both immediate and long-term immunological consequences. Using colony records on a subset of rhesus macaques (Macaca mulatta) inoculated with SIV at the California Primate Research Center, Davis, California, USA, we constructed regression equations to determine whether the animals' psychosocial histories could explain any of the variability observed in measures of disease progression. After controlling for dosage, age at inoculation, sex, and previous inoculation history, psychosocial variables were found to be significantly associated with several indicators of disease, including latencies to display leukopenia and lymphopenia, weight loss, and survival. We believe these preliminary results suggest an important role for psychosocial processes in affecting disease progression in SIV infection in macaques.
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PMID:Psychosocial factors and disease progression in simian AIDS: a preliminary report. 193 Jul 72

Infection with the human immunodeficiency virus (HIV-1) often produces a set of neuropsychiatric dysfunctions which have been termed the AIDS dementia complex. This complex appears due to the infection of brain cells by HIV-1. If so, brain cells might be expected to contain a binding site for the same viral envelope glycoprotein that enables HIV-1 to bind to other cells (e.g. CD4+ T-cells), gp120. The present study shows that the cells of the brain-derived U-138MG, U-373MG, SK-N-MC and SK-N-SH cell lines bind gp120 in an inhibitable fashion. Binding of gp120 to these cells is inhibited by the dyes Aurintricarboxylic acid (ATA) and Evans blue (EB), which are known to inhibit specific gp120 and HIV-1 binding, and block HIV-1 infection, in CD4-expressing cells. Binding is not inhibited by Aurin, a dye related to ATA but lacking its anti-HIV effects. As expected, anti-CD4 antibodies are ineffective in blocking gp120 binding to brain-derived cells. These results suggest that human brain-derived cells possess a specific binding site for gp120 that is not the CD4 antigen.
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PMID:Brain-derived cells contain a specific binding site for Gp120 which is not the CD4 antigen. 193 87

Fungal infections have gained importance recently. The major reason for this is the increasing number of patients with immunodeficiency. Systemic treatment of invasive fungal infections up to now has been based on relatively few antimycotic agents (amphotericin B, flucytosine, as well as the azole derivatives fluconazole and itraconazole). Only a few number of fungi cause the majority of opportunistic fungal infections. Candida albicans leads to severe mucosal infections in cases of immunodeficiency. Systemic mycoses usually present as endogenous infections or are caused by an infected central venous catheter with dissemination into multiple organs. Less severe candida infections should be treated with fluconazole. A more severe candida infection still requires treatment with amphotericin B plus flucytosine. Aspergillus fumigatus, a ubiquitous mold, is the most frequent pathogen in patients with granulocytopenia. First choice treatment also is amphotericin B and flucytosine; treatment should be started despite lacking proof of pathogen in patients with immunodeficiency and typical clinical signs. Itraconazole, the azole derivative active against aspergillus, may be administered only in mild cases of aspergillus infections in immunocompromised patients. Infections with Cryptococcus neoformans, which hardly ever occur, have been observed frequently in AIDS patients. The manifestation of cryptococcosis mainly presents as chronical meningitis. Presently various treatment concepts are being clinically tested. An initial combination of amphotericin B, flucytosine, and fluconazole, followed by long-term treatment with fluconazole, is recommended.
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PMID:[Therapy of systemic mycoses in immunodeficiency]. 193 55

For many years tuberculosis has been known to occur with greater frequency among persons with disorders that impair host defenses. In most instances these processes interfere with the immune response to Mycobacterium tuberculosis, whereas, in a few, such as silicosis, the probable abnormality is a nonimmune defect in macrophage function. Infection with the human immunodeficiency virus (HIV) causes progressive and ultimately profound depression of both humoral and cell-mediated immunity and, thus, is an extremely potent risk-factor for tuberculosis. Presumably the major effect of HIV infection that predisposes persons to developing tuberculosis is the reduction in circulating T-helper (CD4+) lymphocytes which causes a reduction in cytokine production and a consequent decrease in the functional capabilities of macrophages. However, a number of questions concerning pathogenesis of tuberculosis related to HIV remain. Available data suggest that the magnitude of the risk for developing tuberculosis among persons infected with both HIV and M. tuberculosis is very high, 8% in one prospective study. Because of the epidemic of HIV infection, the progressive downward trend in the incidence of tuberculosis in the United States has reversed and in 1989 there was a 5% increase in the number of cases. Preliminary data for 1990 suggest that there will be an 8 to 10% increase over 1989. Also in the United States approximately 3% of tuberculosis patients have been found to be HIV seropositive. The clinical features of tuberculosis in patients with HIV infection vary depending on the degree of immunosuppression. With mild immunosuppression early in the course of HIV infection tuberculosis presents in a "typical" way with positive tuberculin skin tests, upper lobe cavitary infiltrates on chest film and positive sputum smears and cultures. As the HIV infection progresses, the mode of presentation of tuberculosis becomes more "atypical" with negative skin tests, multiple sites of involvement, chest films showing diffuse noncavitary infiltrates often accompanied by intrathoracic lymphadenopathy. The key to diagnosis is maintaining a high index of suspicion for tuberculosis, especially in patients with advanced HIV disease and including appropriate laboratory examinations in the evaluations of such persons. Regardless of the stage of HIV infection the response to treatment for tuberculosis is generally favorable if it is begun promptly. Standard therapy utilizing isoniazid, rifampin, and pyrazinamide with or without ethambutol have been associated with high rates of cure. Relapse has been uncommon. There has been, however, at least one outbreak of tuberculosis caused by isoniazid and rifampin resistant organisms in which the response to therapy was very poor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features, diagnoses, and management of tuberculosis in immunocompromised hosts. 194 27

Mycobacterium haemophilum, previously characterized as an unusual pathogen, is found primarily in immunocompromised hosts. This organism has stringent growth characteristics and may not be isolated using routine techniques. M. haemophilum infects the skin and underlying tissues, a circumstance which reflects the organism's propensity for growth in a cooler environment. Infections have been reported in renal transplant recipients, patients with Hodgkin's disease, and, more recently, patients with AIDS. The organism has also been isolated from children with cervical lymphadenitis in the absence of apparent immunodeficiency. Response to therapy has not been uniform, and in some instances improvement in immune status has been associated with regression of lesions. With proliferation of transplantation surgery, chemotherapy, and AIDS, the number of infections due to M. haemophilum is likely to increase.
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PMID:Mycobacterium haemophilum infection in immunocompromised patients: case report and review of the literature. 196 7

Some strains of mice inoculated with LP-BM5 murine leukemia virus (MuLV) develop a syndrome, termed mouse acquired immunodeficiency syndrome (MAIDS), characterized by progressive lymphoproliferation and profound immunodeficiency. LP-BM5 MuLV is a virus mixture that contains ecotropic (eco) and mink cell focus-induced MuLV and a defective genome that is the proximal cause of disease. Flow cytometry analyses of spleen and lymph nodes from susceptible C57BL/6 mice infected with this virus mixture revealed the presence in spleen and peripheral lymph nodes of a previously unrecognized subset of CD4+CD3+ T cells that are Thy-1-. The frequency of these cells increased with progression of disease, eventually comprising between 30% and 50% of all CD4+ cells. Infection of A/J mice, a strain which is genetically resistant to development of MAIDS, did not induce an increase of this T cell population, indicating that infection with the virus mixture was insufficient to induce its proliferation. A central role for the defective virus in this process was suggested by the finding that C57BL/6 mice infected with LP-BM5 eco alone did not have increased frequencies of Thy-1-CD4+ cells in spleen. Studies of spleen and peripheral lymph node cells from normal mice demonstrated the presence of Thy-1-CD4+ cells at frequencies of 1%-2%. Studies using two anti-T cell monoclonal antibodies, SM6C10 and SM3G11, that define four CD4+ subsets showed that Thy-1-CD4+ T cells from normal and infected mice were present only in the 6C10- subsets.
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PMID:A unique subset of normal murine CD4+ T cells lacking Thy-1 is expanded in a murine retrovirus-induced immunodeficiency syndrome, MAIDS. 198 Jan 14


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