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)

Plagemann, Peter G. W. (Western Reserve University, Cleveland, Ohio), and H. Earle Swim. Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell. J. Bacteriol. 91:2317-2326. 1966.-The replication of mengovirus was studied in two strains of Novikoff (rat) hepatoma cells propagated in vitro. The replicative cycle in both strains required 6.5 to 7 hr. Infection resulted in a marked depression of ribonucleic acid (RNA) and protein synthesis by strain N1S1-63. Inhibition of RNA synthesis was reflected by a decrease in the deoxyribonucleic acid (DNA)-dependent RNA polymerase activity of isolated nuclei. Mengovirus had no effect on either protein or RNA synthesis or on the DNA-dependent RNA polymerase activity of a second strain, N1S1-67. The time course of viral-induced synthesis of RNA by cells was studied in cells treated with actinomycin D. It was first detectable between 2.5 and 3 hr after infection and continued until 6.5 to 7 hr. The formation of mature virus was estimated biochemically by measuring the amount of RNA synthesized as a result of viral infection which was resistant to degradation by ribonuclease in the presence of deoxycholate. Approximately 70% of the deoxycholate-ribonuclease-resistant RNA was located in mature virus, and the remainder was double-stranded. The formation of mature virus began about 45 min after viral-directed (actinomycin-resistant) synthesis of RNA was detectable in the cell, and only about 18 to 20% of the total RNA synthesized was incorporated into virus. Release of virus from cells began about 1 hr after maturation was first detectable. Release of virus from cells was accompanied by a loss of a large proportion of their cytoplasmic RNA and protein.
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PMID:Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell. 428 85

Rinderpest virus infection was shown to induce marked suppression of both humoral antibody response and cell-mediated immunity in rabbits. The virus exhibited a suppressive effect on primary antibody response as indicated by a decrease in numbers of plaque-forming cells (immunoglobulin [Ig]M) and hemagglutinating antibody titers of both IgM and IgG types to sheep red blood cells, whereas there was no detectable effect of the virus on the production of memory cells. Virus-induced suppression of cell-mediated immunity was demonstrated by a decreased rate of proliferative response of peripheral lymphocytes to phytohemagglutinin stimulus and by a depression of delayed-type skin reactions to purified protein derivative. Such suppressive effects were indicated to persist for 14 days or longer. Alteration in phagocytic activity of the reticuloendothelial system was not observed. The relevance of the virus-induced histological lesions in the lymphoid tissues to the virus-induced immunosuppression was discussed.
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PMID:Pathogenesis of rinderpest virus infection in rabbits. II. Effect of rinderpest virus on the immune functions of rabbits. 459 40

Effects of altered gaseous environments (parabarosis) on interferon production in mice were studied, with Newcastle disease virus (NDV) as the inducer. Increased levels of interferon in lung tissue were observed when mice were exposed to 11% O(2) in N(2) for 3 days before and after, or only after, injection of NDV. However, serum interferon levels remained unchanged. Exposure of mice to 77% O(2) for up to 7 days did not affect the response to interferon induction as assayed in lungs or sera. Interferon levels were significantly depressed in mice exposed to a simulated depth of 213 ft in seawater [with normal partial pressure of O(2) (pO(2)) in N(2)] for 2 or 4 weeks. Whereas definite depression of interferon was also observed in mice maintained at a simulated altitude of 37,000 ft (with normal pO(2)) for 2 weeks, those maintained at the same condition for 4 weeks showed a normal level of interferon. The results obtained with hypoxia are compatible with other reports on the influence of O(2) tension on viral infection. The factors responsible for alterations observed in interferon level in mice kept in normal pO(2), but under altered pressure, have not yet been identified.
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PMID:Production of interferon in mice: effect of altered gaseous environments. 568 5

Polymorphonuclear leucocytes function--Gey mobility, chemotaxis, NBT and myeloperoxidases--was studied in 29 patients with active viral infection and after clinic recuperation: 19 mumps meningitis, five measles, three varicella, one adenovirosis and one hepatitis A; these patients were compared with 31 age matched controls. Gey mobility and chemotaxis was markedly depressed during the acute period (p [0.05 and p less than 0.001 respectively), returning to normal values with clearing of infection. Also, myeloperoxidase decreases during acute period (p less than 0.05), but they don't return to normal values with clinic recuperation (p less than 0.05). NBT was similar in both groups. Studying mumps meningitis alone authors observed that results were similar to before: chemotaxis deficit (p less than 0.05) and myeloperoxidases (p less than 0,01). According to these results depression of polymorphonuclear function justifies only partially the higher predisposition to bacterial superinfection that some viral infections have.
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PMID:[Reduction of the function of polymorphonucleocytes: chemotaxis and myeloperoxidases in viral infections in childhood]. 609 60

Effector mechanisms responsible for protection against ectromelia virus (EMV) including antiviral activity of non-immune macrophages, cytotoxic T cells, antiviral antibody, delayed footpad reaction to viral antigen and interferon induction after viral infection were depressed in BALB/c mice bearing syngeneic Meth A tumors. The degree of viral growth correlated well with the depression of delayed footpad reaction, antibody production and interferon induction. But a control level of these elements could be obtained by pretreatment of tumor-bearing mice, with PSK Cytotoxic activity may not be the principal effector, since cytotoxicity was induced in both normal and tumor-bearing mice to almost the same extent but an explosive viral growth was observed only in the latter. These results suggest that PSK was responsible for restoring the depressed antiviral protective immunity to normal levels in tumor-bearing animals.
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PMID:[Depression of protective mechanisms against ectromelia virus infection in tumor-bearing mice and its prevention by PSK]. 609 65

The influence of herpes zoster virus infection on cell-mediated and humoral immunity to varicella-zoster virus (VZV), cytomegalovirus, and herpes simplex virus (HSV) was followed in 17 zoster patients from the first week to 6 months after start of eruptions. The clinical responses were registered and correlated to the immune responses. A significant depression in blast transformation on stimulation of lymphocytes with all three antigens was found on days 1 to 5 compared with transformations later after zoster eruptions and compared with controls. Phytohemagglutinin exhibited the same stimulation in the different groups and controls. No significant differences in interferon production in the various groups and controls were found on stimulation with the VZV and HSV antigens. All zoster patients became seropositive by complement fixation to VZV a few days after start of the zoster eruption. Two zoster patients showed a fourfold rise in complement fixation antibodies to HSV. Three patients had changes in complement fixation titers to cytomegalovirus, which could indicate new infection or reactivation of infection with this virus. A significant lower transformation index to VZV was found during the first 9 days in zoster patients with fever compared with patients without fever. The relevance of this observation is discussed in relation to a previous similar observation from our group.
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PMID:Cell-mediated and humoral immunity to herpesviruses during and after herpes zoster infections. 616 9

Renal transplant recipients receiving low maintenance immunosuppression (azathioprine, 2 mg/kg/day, and prednisolone, 10 mg/day), tolerating their transplants well, and without viral infection disclose a profound depression of NK activity as assessed by 51Cr-release assay. By combining the analysis of the different steps of cytolysis with the agarose single-effector assays and the estimation of circulating large granular lymphocytes (LGL), the defect is shown to be due to a significant decrease of the number of NK cells capable of binding (% target-binding cells 2.0 +/- 0.3 versus 5.7 +/- 0.7 in normals, P less than 0.001) and killing (% cytotoxic target-binding cells 12.4 +/- 1.9 versus 22.0 +/- 0.5 in normals, P less than 0.001) of targets. There is also a significant reduction (P less than 0.001) of both percentages (1.0 +/- 0.2 versus 3.3 +/- 0.4 in normals) and absolute values (9.8 +/- 2.4 versus 62.3 +/- 8.0/microliters in normals) of LGL. These observations indicate that depressed NK activity is due mostly to depletion of NK cells. Functional impairment of NK cells can also be involved. Lack of direct in vitro effects of drugs (6-mercaptopurine, hydrocortisone, and methylprednisolone) at concentrations likely to be reached in vivo during treatments and relative resistance of NK activity after in vivo steroid administration suggest that immunosuppressive drugs act at the precursor cell level or on regulatory mechanisms. Despite functional integrity of two suppressor cell systems of allogeneic NK activity (suppression induced by preculture of lymphocytes with Con A and suppressor granulocytes) in immunosuppressed patients, tested on normal NK cells, NK cells of immunosuppressed patients did not disclose greater susceptibility to Con A-induced suppression. This analysis indicates that the depletion phenomenon is probably a major mechanism in NK depression of patients receiving immunosuppressive drugs.
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PMID:Deficient natural killer function in patients receiving immunosuppressive drugs: analysis at the cellular level. 623 88

Myocrisin given to mice i.p. causes depression of lysosomal enzyme activity (acid phosphatase, beta-glucuronidase and N-acetyl-beta-D-glucosaminidase) in peritoneal macrophages. If avirulent Semliki Forest virus (SFV) is given i.p. 3 h after the Myocrisin, further depression of lysosomal enzyme activity occurs, a very high titre of virus is produced in these macrophages and the virus becomes lethal, causing 100% mortality. The possible interrelationships between depressed lysosomal activity, high virus titres and the production of a lethal virus infection are discussed.
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PMID:Lysosomal enzyme changes in macrophages from mice given myocrisin and infected with avirulent Semliki Forest virus. 629 31

Experiments were performed on 12-wk-old nonobese diabetic (NOD) mice to investigate the immunologic background of the condition, using ICR mice as controls. The results indicate the following: (1) absolute decreases in number of T lymphocytes, (2) depression of natural killer activity, (3) normal responsiveness in delayed type hypersensitivity and functional depression of killer T cells against allogeneic tumors, (4) diminished resistance to herpes virus infection, and (5) enhanced production of polyclonal antibodies to T cell-dependent antigens. These features are similar to those noted in other autoimmune diseases of man and in their experimental models in laboratory animals. Elucidation of the pathogenetic mechanism of autoimmune diabetes mellitus in NOD mice, therefore, may contribute to the diagnosis, treatment, and prevention of a wide variety of autoimmune diseases.
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PMID:Immunologic aspects of the nonobese diabetic (NOD) mouse. Abnormalities of cellular immunity. 629 42

By their position at sites of initial infection and their wide distribution in major organs of the body, macrophages may be decisive in determining the susceptibility or resistance of the host to virus infection. Macrophage restriction of virus replication has been shown to be closely related to virus strains or virus types and to the age of the infected host. We report the effects of the development of a solid tumor in rats on intrinsic in vitro macrophage activity against herpes simplex virus type 1. The results obtained with the infectious center assays and the analysis of single-cycle growth curves of herpes simplex virus type 1 in macrophages obtained from normal and tumor-bearing rats showed a depression of antiviral activity of macrophages from tumor-bearing rats. The possibility of immunomodulation by bacterial adjuvants on tumor-bearing rats and the effects on the antiviral activity of peritoneal macrophages were furthermore demonstrated.
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PMID:Tumor-dependent resistance of rat peritoneal macrophages to herpes simplex virus. 629 45


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