Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from 37 Nigerian men with Kaposi's sarcoma were examined for evidence of infection with human T-cell lymphotropic virus type III (HTLV-III), cytomegalovirus (CMV), Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis A virus (HAV), and Candida albicans. For comparison purposes, sera from 30 patients with primary cell liver carcinoma and 150 health young adults were also assessed. The Kaposi's sarcoma patients were in poor general condition, with severe anemia and gross sepsis. In each case, cutaneous disease affected only the limbs-- a finding that is in contrast with the visceral organ involvement seen in most black African victims. The serologic testing provided clear evidence that tropical African Kaposi's sarcoma is not associated with HTLV-III infection; non of the 217 serum samples analyzed from the 3 study groups showed antibodies to this virus. A widespread pattern among the Kaposi's sarcoma and liver carcinoma patients was depression of peripheral blood monocyte chemotaxis and a diminished, delayed-type hypersensitivity reaction to tuberculin. All patients in these 2 groups demonstrated circulating antibodies to CMV, EBV, HBV, AND HAV. Candida albicans was isolated from 30 of the 37 Kaposi's sarcoma patients and all 30 liver carcinoma patients compared with none of the health controls. These findings suggest that endemic tropical African Kaposi's sarcoma is a different disease than the epidemic AIDS-linked Kaposi's sarcoma reported from the US, and it is probable that different etiologic agents are involved in each case.
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PMID:Kaposi's sarcoma and HTLV-III: a study in Nigerian adult males. 302 63

A considerable strain difference was noted in BALB/c and C57BL/6 mice with regard to the impairment of antibody responses to poliovirus antigens in the course of infection with murine cytomegalovirus (MCMV): a long lasting reduction in antibody formation in BALB/c mice contrasted with an only moderate depression observed in C57BL/6 animals. Analysis of antibody classes and IgG subclasses revealed that anti-poliovirus VP1 antibodies in BALB/c mice were predominantly of the IgG3 subclass, a subclass most drastically affected by MCMV infection, while C57BL/6 mice produced antibodies of the IgM class and of IgG1 and IgG2 subclasses which were reduced to a lesser extent by the infection with MCMV. It is concluded that the strain difference observed may be explained on the basis of differences in the handling of poliovirus antigenic determinants by BALB/c and C57BL/6 mice.
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PMID:Anti-poliovirus IgG subclass antibodies in cytomegalovirus infected mice. 302 34

This article discusses clinical, immunologic, and etiologic considerations in the acquired immunodeficiency syndrome (AIDS) and the relationship of AIDS to other immunodeficiency diseases. The outstanding clinical feature of AIDS is the occurrence of opportunistic infections in individuals with no prior known cause of immunodeficiency. Such infections have included Pneumocystis carinii, oral thrush from Candida albicans, cytomegalovirus, atypical mycobacteria, cryptosporidium, and Herpes simplex virus. Central nervous system invasion by Cryptococcus neoformans and Toxoplasma gondi has also been reported. Persistent quantitative and functional depression of T4 cells is the immunologic hallmark of full-blown AIDS. Another prominent feature is in vitro spontaneous hyperactivity of B cells. AIDS patients lose cutaneous delayed hypersensitivity reactions both to recall and to new antigens, and T-cell-mediated cytotoxicity is diminished. The mounting number of T8 cells and diminution in T4 cells causes an inversion in the normal T4:T8 ratio. It has been hypothesized that the host defense mechanism is the attempt of the cytotoxic T8 cells to destroy the virus-infected T4 cells. 2 groups of investigators have discovered a lymphocytotropic retrovirus from blood and node lymphocytes of AIDS patients: lymphadenopathy-associated virus (LAV) or human T-lymphotropic virus type III (HTLV-III). Among the primary immunodeficiencies, AIDS most closely resembles the defect observed in purine nucleoside phosphorylase deficiency, an inherited autosomal recessive phenomenon. There is evidence that multiple infections or antigen overload characterize all the risk groups for AIDS. Moreover, antigen overload in experimental animals and man has been shown to suppress immune responses and to down-regulate Ia antigen expression on monocytes. This may prove to be a necessary precondition for the development of AIDS.
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PMID:The acquired immunodeficiency syndrome (AIDS). 315 26

The epidemic form of Kaposi's sarcoma (KS) that occurs in patients with the acquired immune deficiency syndrome (AIDS) produces lesions that, histopathologically, are indistinguishable from those of classical KS or of the endemic form of the disease seen in children and adults in certain areas of Africa. There are, however, important differences in the pathogenesis of the disease in the different groups affected by the neoplasm. Compared with classical KS in people of eastern European and Mediterranean descent, which commonly takes a protracted, indolent course, the epidemic Kaposi's sarcoma (EKS) is far more aggressive. However, the KS seen in adults in endemic areas of Africa may also become florid and rapidly progressive after years of quiescence. Some degree of immune dysfunction is thought to be a factor in all forms of KS, with immune depression being the hallmark of EKS and the setting in which it occurs. Cytomegalovirus (CMV) is thought to be at least a cofactor in the disease, but it has also been suggested that the etiologic agent of AIDS, human immunodeficiency virus (HIV), may also play a role in EKS.
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PMID:Pathophysiology and epidemiology of epidemic Kaposi's sarcoma. 329 18

Thirty-nine renal allograft recipients were prospectively studied to determine the quantitative effects of different immunosuppression protocols on T-cell subsets (total lymphocytes [T3], helper/inducer [T4] and suppressor/cytotoxic [T8]). Eighteen patients were initially immunosuppressed with only azathioprine and prednisone but required subsequent treatment for rejection by the addition of antithymocyte globulin (ATG) (Upjohn, Kalamazoo, MI) or conversion to cyclosporine. Three of these patients had ATG-resistant rejections and were treated with the monoclonal antibody ORTHO OKT3 (ORTHO Pharmaceuticals, Raritan, NJ). Twenty-one patients were treated only with cyclosporine and prednisone. Plasma levels of cyclosporine, as determined by high-performance liquid chromatography, were kept in the range of 50-100 ng/mL (mean: 78.1 +/- 52.1). One patient had a lymphoma, two patients had failed grafts, and three patients converted their cytomegalovirus titers. The results demonstrate that the immunosuppressive agents, azathioprine, prednisone, and cyclosporine, have an additive effect in depressing the T-lymphocytes and their subsets. In addition, ATG and cyclosporine had a more selective ablation of the T4 subset, resulting in a reversal of the T4/T8 ratios. This depression was independent of the plasma level of cyclosporine. Finally, the pan T-cell monoclonal antibody OKT3 led to severe depletion of all T-cell subsets but resulted in a normal T4/T8 ratio. In conclusion, immunosuppressive agents have a variable effect on T-lymphocytes and their subsets that cannot be adequately characterized by the T4/T8 ratio alone, but which should be quantitatively assessed by examining all subsets.
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PMID:T-lymphocyte subsets in renal allograft recipients treated with cyclosporine and azathioprine. 354 1

A 53-yr-old Chinese sailor developed prolonged pyrexia with unresolved lobar pneumonia, cervical lymphadenopathy, generalized subcutaneous abscesses, and pericardial effusion. Penicillium marneffei was isolated from pericardial fluid and subcutaneous pus and was demonstrated on histologic sections of lymph nodes and lung tissue. The penicilliosis was treated successfully with amphotericin B, ketoconazole, and 5-fluorocytosine. Subsequently, he also developed other T-lymphocyte-related opportunistic infections such as disseminated cutaneous herpes zoster and chronic osteomyelitis of sternum caused by Salmonella typhimurium. He was also a chronic carrier of cytomegalovirus. Further investigations showed that he had persistent depression of T-lymphocyte function and enhancement of B-lymphocyte activity, the cause of which was undetermined.
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PMID:A case of invasive penicilliosis in Hong Kong with immunologic evaluation. 387 95

Macrophages infected in vitro with murine cytomegalovirus (MCMV) manifest depressed phagocytic uptake of a variety of particles within hours after the initiation of infection. Analysis of kinetics of uptake of radiolabeled Staphylococcus aureus by MCMV-infected macrophages indicates that the diminished uptake results from a depression in the calculated maximum velocity of uptake (Vmax) with the apparent Michaelis constant (KM) remaining unaltered. This pattern of altered uptake is typical of that seen after manipulations that affect the surface interactions of macrophages with ingestible particles. Coincubation of macrophages and radiolabeled Staphylococcus with opsonizing antibody resulted in normalization of the phagocytic rates. The surface localization of the defective phagocytosis was further confirmed by light and scanning electron microscopy of the macrophages incubated with Staphylococcus or latex spherules. These data indicate that defective macrophage surface that interferes with the initial macrophage-particle interactions that initiate nonimmune phagocytosis.
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PMID:Murine cytomegalovirus-induced macrophage dysfunction. 608 99

The nonspecific functional capacity of spleen cells, taken from female guinea pigs with primary acute cytomegalovirus (CMV) infection, was assessed using lipopolysaccharide (LPS), a B-cell mitogen, and concanavalin A (Con A), a T-cell mitogen. Proliferative responses to the two mitogens were found to be significantly depressed in animals inoculated with CMV as compared to control animals. The defect in Con A responsiveness occurred earlier during the course of the infection than the defect in LPS responses. Although responses to the mitogens were depressed at the time of peak virus activity in the spleen, the possibility of lytic destruction of the spleen cells by the virus during in vitro culture was excluded. In addition, the depression in Con A responsiveness was noted with a wide range of Con A concentrations, and preculture studies failed to result in enhanced reactivity of the cells from infected animals. We conclude that reductions of both B- and T-cell functions, which differ in their timing during the course of acute CMV infection, occur concurrently with an enhanced viral specific immune response in guinea pigs acutely infected with CMV.
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PMID:Asynchronous depression of responses to T- and B-cell mitogens during acute infection with cytomegalovirus in the guinea pig. 608 91

In mice treated with ordinarily sublethal doses of parathion 2 to 5 days postinfection with murine cytomegalovirus (MCMV) 50 to 100% mortality was observed. These mortalities appeared to be due to a decrease in the ability of infected mice to detoxify parathion. Pentobarbital-induced sleeping time was also enhanced 3 and 6 days postinfection and cytochrome P-450 concentrations were markedly depressed in mice tested 3 days after infection. MCMV-induced effects on sensitivity to parathion and pentobarbital did not appear to be directly attributable to liver infection since concentrations of virus in the liver persisted at maximum concentrations well beyond the time when sensitivity to these compounds returned to normal. The time frame during which enhanced sensitivity to parathion and pentobarbital was observed suggests that this sensitivity may have been caused by viral-induced interferon-mediated depression of cytochrome P-450.
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PMID:Increased susceptibility to parathion poisoning following murine cytomegalovirus infection. 609 89

A 31-year-old Frenchman had an acquired immunodeficiency syndrome (AIDS) with profound depression of cellular immunity and relative sparing of humoral immunity. The clinical picture included intractable secretory diarrhoea, vomiting, abdominal pain, and weight loss. Gastrointestinal cryptosporidiosis was present and a perfusion technique showed profuse secretion of fluid in the proximal small bowel. The patient also had recurrent Salmonella typhimurium septicaemia, cytomegalovirus infection, and cerebral toxoplasmosis and he died within 13 months. This patient did not belong to any of the groups known to be affected by this type of acquired immunodeficiency (homosexuals, drug addicts, haemophiliacs, Haitians) but had been transfused with Haitian blood 4 years before onset of symptoms. This case supports the notion that some forms of AIDS may be transmitted by blood, with a long incubation period.
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PMID:Acquired immunodeficiency with intestinal cryptosporidiosis: possible transmission by Haitian whole blood. 613 90


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