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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both in vitro and in vivo murine cytomegalovirus (MCMV) infection depressed the responses of lymphocytes to both B and T cell mitogens. The possibilities that macrophages or nonspecific T cell inhibition of B cells might account for the depressed responses were eliminated. In vitro data suggested that B cell responses are more susceptible to this depression than T cell responses. The possibility that the depression of T cell responses is not a direct effect of viral infection of lymphocytes is discussed. To investigate further the interaction between B and T lymphocytes and MCMV, mice with B and T cell deficiences were studied. A comparison of the susceptibility of athymic Nu/Nu mice and T cell competent Nu/+ littermates to MCMV showed that the LD50 for Nu/Nu mice is 10-fold lower than that for Nu/+ mice, but Nu/+ mice given an LD50 of virus died much sooner after infection than Nu/Nu mice given an LD50. Pathogenic mechanisms responsible for death may be different in these two groups of mice. Similarly the MCMV LD50 for B cell-deficient mice (treated with goat anti-mouse IgM serum) was 10-fold lower than the LD50 for mice treated with normal goat serum, but given an LD50 of virus, the latter died sooner after infection than the former. In contrast, there was little difference between the LD50 or time of death after MCMV infection of CBA x DBA F1 male mice (which are deficient in their response to thymic independent antigens) and their normal littermates, the CBA x DBA F1 female mice.
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PMID:Effect of murine cytomegalovirus on the in vitro responses of T and B cells to mitogens. 17 97

Groups of mice that received a predominantly lethal or a nonlethal dose of murine cytomegalovirus (CMV) were studied prospectively to correlate clinical observations with detection of virus in spleen cells and with the response of spleen cells to the thymus-derived (T-) cell mitogen concanavalin A (con A). In both groups of mice, virus was virtually cleared from spleen cells by day 8 after infection. Depression of the spleen cell response to con A preceded clinical signs of infection, was more severe in the lethally infected group, and improved as clinical signs cleared in the few surviving mice. Serum from infected mice depressed the response of uninfected spleen cells to con A. These findings support the hypothesis that clinical illness and death from CMV infection of mice are a consequence of events that follow the depression of T-cell function by CMV. This depression is at least partially mediated by a humoral mechanism.
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PMID:Progressive inhibition of T-cell function preceding clinical signs of cytomegalovirus infection in mice. 19 44

An ongoing prospective study of the role of viruses in renal transplant recipients has provided identification of two patterns of cytomegalovirus (CMV) infection. In both patterns, fever and leukopenia occur within 6 months after transplant. In addition, the benign form is characterized by renal biopsy evidence of rejection and brisk Antibody responses to CMV. The lethal syndrome runs a typical 4 week course, beginning with prostration, orthostatic hypotension, mild hypoxemia and progressing to severe pulmonary and hepatic dysfunction, muscle wasting, central nervous system depression, and death. antibody responses to CMV are minimal, and renal biopsy does not show rejection despite elevation of serum creatinine. At autopsy, CMV is found in lung, liver, kidney, gastrointestinal tract, and brain. Successful management of the potentially lethal kidney, gastrointestinal tract, and brain. Successful management of the potentially lethal CMV syndrome requires rapid clinical recognition and immediate reduction of immunosuppressive therapy. future prospects for control include development of a CMV vaccine and specific antiviral chemotherapy.
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PMID:Clinical characteristics of the lethal cytomegalovirus infection following renal transplantation. 19 56

A prospective study of 15 patients who received renal transplants defined the effect of renal transplantation on the cellular immune response to cytomegalovirus infection. Of 15 patients, 14 developed cytomegalovirus infection, usually in the first 2 months after transplantation, and all infections were accompanied by a normal humoral immune response. After the initiation of immunosuppressive therapy and transplantation, there was a general depression of lymphocyte transformation, as reflected in the response to phytohemagglutinin, accompanied by a specific defect in cellular immunity, as indicated by lymphocyte transformation to cytomegalovirus antigen. Eleven patients had cellular immunity to cytomegalovirus before transplantation, and all of these became negative in the first month after transplantation. In subsequent months, only 6 of the 14 study patients with cytomegalovirus infection developed specific cellular immune responses to cytomegalovirus. This occurred most often in patients who had severe febrile illnesses in association with infection. The specific cellular immune response which developed in the posttransplant period did not persist in three of the patients. This study demonstrates the dissociation of the humoral and cellular immune response to cytomegalovirus infection in renal transplant patients and indicates the importance of the loss of cellular immunity in the appearance of infection. Previously infected patients lost their cell-mediated immunity and had reactivation infections despite the presence of serum antibody.
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PMID:Cellular immune response to cytomegalovirus infection after renal transplantation. 21 41

The specific cellular immune response against Cytomegalovirus (CMV) was studied by the Leucocyte Inhibitory Factor (LIF) production test in three groups of subjects: 7 healthy individuals with no CMV antibodies, 4 with antibodies to CMV but without evidence of active infection, and 2 children with clinical CMV infection. Our results show that LIF production in presence of CMV is high in normal seropositive subjects, while it is strongly deficient in patients with active infection, despite a good humoral response to the virus. In one child with congenital infection, a low number of E rosette forming cells was also revealed. We suggest that CMV infection can induce, at least during infancy, a state of specific cellular unresponsiveness to the virus. When the infection is congenital, a generalized depression of the cellular immune system may develop.
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PMID:Specific cellular unreactivity during cytomegalovirus infection in man. 21 76

Cell-mediated immunity to herpes simplex virus and cytomegalovirus, using the lymphocyte transformation test and interferon induction in lymphocytes, was studied in 59 patients from 1 day to 7 years after allotransplantation and compared with the results in normal subjects. Both parameters were permanently depressed with regard to cytomegalovirus. With herpes simplex virus, interferon production was also permanently depressed, whereas the transformation reaction was normal during the first year after transplantation and only slightly depressed in patients more than 1 year after transplantation. In 6 patients the above-mentioned assays and the complement fixation reaction were performed serially and related to the clinical signs of herpes simplex virus and cytomegalovirus infection. The relationship between depression of the transformation reaction and interferon production in lymphocytes and the occurrence of clinically evident herpes simplex virus and cytomegalovirus infections was, however, equivocal. The humoral immune response to herpes simplex virus was measured by the complement fixation test and the more sensitive antibody-dependent, cell-mediated cytotoxicity reaction, and a good correlation was found between these two tests, although only a few persons were found to be negative in the antibody-dependent, cell-mediated cytotoxicity reaction. The suggestion is made that only a few adults are "true" herpes simplex virus seronegative.
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PMID:Cell-mediated and humoral immune responses to herpes simplex virus and cytomegalovirus in renal transplant patients. 22 63

The purpose of this study was to compare the effects of murine cytomegalovirus infection introduced after an EL4 ascites tumor allograft with cytomegalovirus infection accompanying or preceding the allograft. Parameters that were measured included documentation to the host's immune system. Depressed immune response of splenocytes from mice infected at any time before assay was documented by decreased responsiveness to phytohemagglutinin, to lipopolysaccharide, and to an alloantigen in mixed lymphocyte culture. In contrast, animals infected after grafting had enhanced lymphocyte-mediated cytolysis (LMC), enhanced serum-mediated cytolysis (SMC), and larger spleens than did animals that were only grafted and animals that were infected before grafting. Neither a depressive nor an enhancing effect of virus administered after grafting was reflected in vivo in reduced or increased graft clearance. Nonspecific effects of virus increased LMC and SMC in vitro, but the primary effect of viral infection after grafting is immune depression.
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PMID:Effects of murine cytomegalovirus infection on the immune response to a tumor allograft. 23 71

Sixty-eight patients of clinically diagnosed myocarditis, 0--15 years of age, were followed up and analyzed. Forty (58.8%) were males. The majority were older than 5 years. Clinical courses were rather mild, chronic and self-limiting at large. Only 1 case had a relation to chronic cariomyopathy. Exertional symptoms (chest pain, chest distress, syncope) were seen in 25 (36.8%). ECG changes were very common: the majority were nonspecific ST elevation, depression or both, mainly in leads II, III, V5 and V6. Positive Master' test, prolonged QTc, widened mean spatial QRS-T angle and various arrhythmias were also observed. Cardiac performance, estimated by echocardiogram and phono-mechanocardiogram was lowered in 41 (60.3%). Large IV sound and large A wave in apexcardiogram were also frequently found. All but 3 patients showed continuous elevation of serum enzymes, namely, LDH, LDH-1/LDH-2, CPK, CPK-MB, HBD and GOT. Etiological evidences were obtained by serological study in 11 cases (16.2%): 2 of Coxsackie B-1, 3 of Coxsackie B-2, 1 of Coxsackie B-4, 2 of mycoplasma pneumoniae, 1 of cytomegalovirus, 1 of ECHO-7 and 1 of rubella. We proposed a criteria for diagnosis of myocarditis as follows: (1) Exertional symptoms. (2) ECG findings. (3) Serum enzyme abnormality. (4) Lowered cardiac performance. (5) Cardiomegaly. (6) Changing character of all signs and symptoms.
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PMID:Clinical aspects of nonrheumatic myocarditis in children. 47 Jan 4

Fifteen patients with chronic hepatitis B were treated with adenine arabinoside (Ara-A) or human leukocyte interferon (HLI). Cellular immune response to hepatitis B virus surface antigen and antigens prepared from herpes simplex virus, varicella zoster virus, and cytomegalovirus was measured by a lymphocyte blast transformation assay and an assay for interferon production. Measurements were made before, during, and after antiviral treatment. Unlike patients convalescing from acute hepatitis B, only 2 of 15 patients with chronic hepatitis B had significant blast transformation to hepatitis B surface antigen. One such response occurred during the pretreatment period of HLI therapy, and the other was in a patient undergoing low-dose (<10(5) U/kg per day) HLI therapy. Mononuclear cell cultures were tested for interferon production in the presence of hepatitis B surface antigen. Cells from only 1 of 15 patients produced detectable levels of interferon. In contrast, all of these patients had normal cellular immune responses to herpesvirus antigens. Transformation responses to herpes antigens decreased three- to fivefold after patients were treated with >10(5) U of HLI per kg per day. Antiviral therapy with <10(5) U of HLI per kg per day or Ara-A did not produce a detectable depression of transformation response. Ara-A produced marked lymphocytopenia and a marked lymphocyte fragility after 5 or more days of therapy. In vitro Ara-A was toxic to lymphocytes at concentrations as low as 0.5 mug/ml. These changes in lymphocyte parameters may affect the outcome of antiviral therapy.
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PMID:Effects of interferon and adenine arabinoside treatment of hepatitis B virus infection on cellular immune responses. 53 59

Using the clearance of microaggregated iodinated human serum albumin reticuloendothialial system (RES) phagocytic function was tested in 48 long-term renal allograft recipients and was found to be defective at the time of testing in 70%. Depression of RES phagocytosis could be related to total steroid dosage in the previous year and to the patients liability to bacterial infections. Evidence from this test does not suggest an immunosuppressive effect of cytomegalovirus. However, three patients are discussed who have developed chronic active hepatitis that is not due to type B virus.
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PMID:Altered reticuloendothelial function in long-term renal allograft recipients. 79 69


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