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)

Two groups of rhesus monkeys were inoculated with either 10(5) (group 1) or 10(3) (group 2) plaque-forming units of Machupo virus, the etiologic virus of Bolivian hemorrhagic fever. The monkeys were observed for clinical signs; body temperatures, viremias, hematologic changes, and virus-neutralizing antibody were measured. The onset of clinical signs for groups 1 and 2 occurred on days 4-6 and 7-10, respectively, with fever, anorexia, and depression. These and other signs became more severe, and all of the monkeys died; the respective mean times to death for groups 1 and 2 were 14.3 and 19.5 days. Hematocrit, neutrophil, and lymphocyte values decreased in both groups until a few days before death and then increased slightly. Viremias in the two groups peaked on days 13 and 16, respectively, and persisted until death; the sole exception was one monkey in group 2 that developed neutralizing antibody by day 21. The response of the rhesus monkey to Machupo virus thus provides a useful model for the study of Bolivian hemorrhagic fever.
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PMID:A rhesus monkey model for the study of Bolivian hemorrhagic fever. 17 62

The effects of infection on various aspects of lymphoid function in gnotobiotic dogs with 2 virulent strains of canine distemper virus (CDV), Snyder-Hill CDV and R252-CDV, were compared. Both infections resulted in a viremia-related lymphopenia which was nonselective in that the percentages of B and T cells remained unchanged throughout the observation period. Nonfatal Snyder-Hill-CDV infection resulted in a transient depression of in vitro lymphocyte responses to phytohemagglutinin-P, whereas R252-CDV produced prolonged in vitro suppression of phytohemagglutinin-P stimulation. The differences observed are of minor significance and do not explain the differences in central nervous system demyelinating potential between these 1 strains of CVD.
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PMID:Comparison of canine distemper virus strains in gnotobiotic dogs: effects on lymphoid tissues. 30 24

African green monkeys (Cercopithecus aethiops) are highly susceptible to Bolivian hemorrhagic fever (BHF). Six monkeys were inoculated with 1,000 plague-forming units of Machupo virus, the etiologic agent of BHF. They were observed and monitored for clinical signs, body temperature, viremia, hematologic changes, and virus neutralizing antibody. Onset of fever, anorexia, and depression was noted on days 3 to 6 postinoculation. These and other signs increased in severity and all monkeys died: 5 of 6 died by day 13 and one survived until day 24. The median time to death for the group was 12.5 days. The mean value for hematocrit determinations gradually decreased to 30 on day 10 but subsequently increased. Mean neutrophil and lymphocyte values increased slightly until day 3, and then decreased to minimal values of 3,000 and 2,000, respectively, on day 10. Four monkeys were viremic by day 7 and all were viremic on day 10. The monkey that survived until day 24 had a neutralizing antibody titer of 1:32 on day 14 and appeared to recover from the initial acute illness by day 16. It died following onset of severe neurologic signs on day 23. BHF in the African green monkey is similar to the disease described in two species of macaques.
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PMID:The African green monkey as an alternate primate host for studying Machupo virus infection. 40 63

Although an effective vaccine exists to protect against VEE, not all persons who may be exposed to this disease are likely to be vaccinated. The disease most often presents as a short febrile illness but the convalescence period may be protracted, and death due to encephalitis does occur in a small percentage of those infected. Knowledge of the metabolic alterations which occur during VEE may materially aid in its treatment. Use of the V-198 strain of VEE in the rat produces a uniform model in which to study metabolic alterations. Changes that occur early in the disease include viremia, neutrophilia, a decrease in plasma zinc and transferrin, and increased amino acid uptake into liver. Plasma zinc depression persists into the later stage of the disease, but to a lesser degree. Increases in plasma copper and seromucoid occur late in the disease, concurrent with the development of pronounced encephalitis. Hypoalbuminemia and decreased ketonemia occur during both the early and late stages of the disease. Taken together, these metabolic alterations appear to chronicle the development of VEE in the rat. If these metabolic alterations can be linked to specific pathogenic processes, they may be useful as prognostic indicators, in formulating supportive therapy, and as monitors of potential antiviral therapy.
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PMID:Host metabolic alterations during Venezuelan equine encephalitis in the rat. 62 26

Adult Richardson's ground squirrels were infected with western equine encephalomyelitis virus by intranasal instillation. Mortality followed the instillation of a minimum threshold of 4.7 logs of virus while infection was produced by a dosage of 2.3 logs. The incubation period was from four to seven days, being preceded by a viremic phase. Signs were depression, ataxia and paralysis of the limbs. Highest titres of virus were recovered from the brain and histopathological changes involving the central nervous system included meningitis, vasculitis, perivascular cuffing, gliosis, neuronophagia and neuronal degeneration. The virus was also found in a variety of extraneural tissues. Lesions in extraneural tissues included necrosis of brown fat and an apparent increase in number of Kupffer's cells in the liver. The lymphoid tissue was involved indicating a possible source for viremia. The duration and magnitude of viremia were ample enough to provide virus source for arthropods. The potential for transmission of the virus independent of arthropods was discussed in view of the pathogenesis demonstrated in the experimental infections.
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PMID:Intranasal exposure of the Richardson's ground squirrel to Western equine encephalomyelitis virus. 66 6

As part of an inquiry into possible antecedents of idiopathic cardiomyopathy, acute experimental coxsackie virus myocarditis was studied for late structural and functional sequelae. Myocarditis was induced in 12- and 22-day-old hamsters by inoculation with coxsackie virus B3. Early viremia occurred, followed by virus replication in heart muscle. Maximum peak developed tension (Tpd) of isometrically contracting isolated heart muscle was depressed 17 and 43% in the animals inoculated at 12 days, and studied 18 and 90 days later, respectively, as compared to their uninoculated controls. In both infected groups, less muscle stretch was required to reach the length at which Tpd was produced. Animals studied 180 days after inoculation did not differ from controls. The muscles from animals inoculated at 22 days of age and studied 18 days later showed a 15% depression of Tpd compared to their controls. Glycerinated muscles from this infected group developed 50% less tension than their controls. The muscles of hamsters inoculated with virus at 22 days and studied 90 and 180 days later showed no change in Tpd. The data suggest that contractility and compliance of heart muscle are decreased 18 days after inoculation, but recover by 90 days if the animals are inoculated at age 22 days. However, if the animals are inoculated at a younger age (12 days), depression of myocardial performance persists for at least an additional 90 days. It is concluded that the inflammatory stage of experimental acute coxsackie virus B3 myocarditis in the Syrian golden hamster may be followed by residual alterations in contractile proteins and myocardial function.
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PMID:Heart muscle performance after experimental viral myocarditis. 124

The clinical signs, hematologic changes, serum and fecal virus titers, specific antibody production and the occurrence of histologic lesions were studied in 22 nine-week-old seronegative beagle dogs inoculated by the oral and intravenous route with canine parvovirus. Approximately 30% of the dogs had clinical signs of pyrexia, depression, vomiting, and diarrhea irrespective of the route of inoculation. Events in the dogs inoculated intravenously preceded those in dogs inoculated orally by approximately two days. Only one dog died. Lymphopenia was the most consistent hematologic change. Viremia always preceded the initiation of fecal virus shedding. Viral titers in the serum and feces were significantly greater in symptomatic dogs compared to asymptomatic dogs. Termination of the plasma viremia coincided with the onset of the humoral immune response, but viremia persisted one day longer in symptomatic dogs. The severity of lymphoid tissue and intestinal infection, assessed by tissue immunofluorescence and histology, was also greater in symptomatic dogs. The severity of intestinal disease was highly correlated with the magnitude and duration of viremia.
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PMID:Pathogenesis of canine parvovirus enteritis: the importance of viremia. 298 78

We conducted studies on the peripheral blood of 12 depressed patients with previous diagnoses of mood and/or personality disorders. These patients, and other depressives we observed informally, were resistant to infectious mononucleosis during an epidemic of that illness. All 12 had serologic evidence of a chronic or recrudescent viremia caused by the Epstein-Barr virus (EBV), the infectious agent in infectious mononucleosis. Additional evidence that EBV viremia may be causally related to depression was provided by a strong correlation between the intensity of depressive symptoms and the cellular immune response to the EBV infection.
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PMID:Depression correlated with cellular immunity in systemic immunodeficient Epstein-Barr virus syndrome (SIDES). 300 45

Lassa fever is widespread in West Africa, where the case fatality is about 16% in hospitalized adult patients. The clinical course is highly variable, with a few patients developing severe disease with bleeding, adult respiratory distress syndrome, encephalopathy and hypovolemic shock. We studied 70 patients admitted with suspected Lassa fever to a hospital in Sierra Leone, West Africa. Fourteen patients classified as having severe Lassa fever on the basis of serum aspartate amino transferase (AST) greater than 150 IU/L or viremia of greater than 10(3.6) tissue culture infective dose (TCID) 50/ml were found to have statistically significantly depressed lymphocyte counts when compared with patients with mild Lassa fever (AST less than 150 IU/L or viremia, less than 10(3.6)TCID50/ml), (P less than 0.0001) and with febrile control patients, in whom Lassa infection had been excluded by laboratory criteria (P less than 0.0008). Maximum depression occurred a mean of 10.9 days post onset. Patients with severe Lassa fever also had moderate thrombocytopenia, which was statistically significant when compared with febrile control patients (P less than 0.0003) and this occurred a mean of 10.8 days postonset. The most significant changes were in platelet function, which was markedly depressed in patients with severe Lassa fever (P less than 0.0035 in response to ADP and P = 0.0081 for collagen) when compared with patients with mild Lassa fever, and when compared with febrile controls, (P = 0.0013 for ADP and P less than 0.00001 for collagen). This abnormality was usually maximal on admission to hospital, and probably is an early event, preceding hospitalization in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematologic dysfunction in Lassa fever. 318 37

By monitoring immunobiological parameters known to be influenced by interferon (IFN), the natural killer (NK) cell activity of 10 low replication (anti-HBe) virus B-DNA (HBV-DNA) hepatitis patients receiving rIFN alpha-A, of 5 anti-HBe/delta positive hepatitis patients treated with rIFN alpha-2, and of 6 high replication (HBeAg) HBV-DNA hepatitis patients on lymphoblastoid IFN was followed-up during therapy. Overall, strong and significant (p less than 0.01) shift to increase segregated with the low replication subset; the delta positive subset was non-significantly increased (0.30 greater than p greater than 0.2); the high replication subset was depressed in a nearly significant (0.10 greater than p greater than 0.05) manner. Kinetic studies showed the activation of the first subset to follow an early steep rise and a subsequent plateau as fitted with a quadratic curve (p = 0.02); an early rise and a depression at 2 months delineated a complex cubic model (p = 0.06) in the high replication subset. The profound NK depression was clinically witnessed by a sharp rise of the aminotransferases and following drop of viremia. The study shows that i. discrete patterns of NK response as amenable to mathematical models may associate to differential patterns of virus B replication in patients responding to IFN; ii. point(s) on the NK curve may acquire clinical meaning as they coincide with a consensual or opposite shift of a clinical index.
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PMID:Interferon treatment of chronic hepatitis B surface antigen (HBsAg) carriers. A description of the activation profiles of natural killer cells obtained with different schedules of administration in three subsets of carriers. 343 68


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