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 91 patients with strongyloidiasis in Okinawa prefecture, Japan, were examined for the presence of the concurrent infection with adult T-cell leukemia (ATL) virus by detecting the antibody to ATL-associated virus antigen (anti-ATLA). As high as 73.6% of the patients were found to be positive for the anti-ATLA antibody, whereas in 38 Strongyloides-negative controls, the positive rate was only 18.4% A significant increase of OKT 4+ cells and a decrease of OKT 8+ cells were noted among the patients positive for anti-ATLA antibody. A considerable rise of spontaneous proliferation of peripheral lymphocytes and a depression of mitogen-induced proliferative responses were also found in the patients. The increase of background mitogenesis was considered to be due to the concurrent infection with the ATL virus, but the depressed responses to mitogenic stimuli seemed to have no relation with the presence of the viral infection. The possible contribution of strongyloidiasis as a cofactor predisposing to ATL viral infection or leading the virus carriers to ATL patients was discussed.
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PMID:Concurrent infections with Strongyloides and T-cell leukemia virus and their possible effect on immune responses of host. 273 8

Pseudorabies virus was inoculated intratracheally into sheep to investigate the pathogenesis of pseudorabies virus infection. Clinical signs of pyrexia, depression, frequent swallowing, facial fasciculations, chorea, excessive salivation, mild tympanites, labored breathing and focal pruritus were followed by death Macroscopic lesions were severe focal facial trauma, petechiae in cervicothoracic ganglia and dilated esophaguses. The medulla oblongata and the trigeminal, cranial cervical, cervicothoracic and parabronchial ganglia contained pseudorabies virus and pronounced nonsuppurative inflammatory changes. The neural distribution of lesions and virus suggests that the virus travelled from the respiratory mucosa to the central and sympathetic nervous system by two routes: 1) in the vagus and glossopharyngeal nerves to the medulla oblongata and 2) in the postganglionic fibers to the sympathetic ganglia. The presence of virus in the nasal mucus indicated that horizontal transmission of pseudorabies virus may occur among sheep.
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PMID:Pathogenesis of ovine pseudorabies (Aujeszky's disease) following intratracheal inoculation. 282 May 59

Considerable evidence documents the importance of co-factors, including the immune response, in expression of oncogenicity of tumour viruses. To determine whether a common protozoal infection that can depress lymphocyte function alters manifestations of oncogenic virus infection, a mouse model of Toxoplasma infection with depressed T lymphocyte function was developed. In this model, Toxoplasma depressed blastogenic transformation to the T-cell mitogen Concanavalin A and primary antibody response to sheep red blood cells which requires T cell help. Uninfected and Toxoplasma-infected mice were then infected with Moloney leukaemia or Moloney sarcoma viruses and development of lymphoma and sarcoma were evaluated. Toxoplasma infection, which induced depression of T-cell function, decreased the incidence of Moloney sarcoma virus induced rhabdomyosarcomas but did not alter progression or regression of tumour in those mice that developed tumour. Conjoint infection with Toxoplasma and Moloney leukaemia virus did not increase incidence of lymphoma when compared with incidence of lymphoma in mice infected with Moloney leukaemia virus alone.
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PMID:Influence of Toxoplasma on manifestations of Moloney virus infections. 293 10

Previous studies carried out by others have shown that in utero exposure of mice to chlordane effects a significant depression of cell-mediated immunity (CMI) at 100 days of life without adversely affecting the humoral immune system. In the studies reported herein we assessed the effect of in utero exposure to various doses of chlordane on the response of 38-day-old mice to influenza type A virus infection in terms of relative levels of mortality, mean day of death, and the levels of antiviral antibody in the primary and secondary immune response to the virus. In utero exposure to chlordane effected enhanced survival to influenza type A virus infection relative to mock-treated animals. No significant differences were noted in the mean day of death of chlordane-treated and mock-treated mice. A significant enhancement in the levels of antiviral antibody was noted in the chlordane-treated female mice but not male mice in both the primary and secondary immune response to the virus.
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PMID:Influenza type A virus infection of mice exposed in utero to chlordane; survival and antibody studies. 298 57

Previous studies in our laboratory have documented that in utero chlordane exposure caused a significant enhancement in the survival of the offspring to influenza A virus infection, and a depressed delayed type hypersensitivity (DTH) response to oxazolone. To correlate these 2 effects, we assayed influenza A virus-specific DTH response, and found that it was significantly decreased in chlordane-treated offspring. Virus-specific T-cell blastogenesis was also assayed in chlordane-treated animals. No significant differences due to the chlordane treatment were found in virus-specific T-cell blastogenesis, suggesting that the DTH depression did not result from a paucity of antigen-reactive T-cells. To determine whether enhanced survival was due, in part, to the effects of chlordane on virus replication, rather than on immunological alteration alone, the kinetics of influenza virus replication in the lungs of chlordane- and vehicle-treated animals were determined. In utero chlordane treatment caused no significant differences in in vivo virus replication. These data suggest that increased survival was due to a decrease in virus-specific DTH and its associated pathology.
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PMID:The effect of prenatal chlordane exposure on specific anti-influenza cell-mediated immunity. 299 71

Recent data indicate that the lymphadenopathy-associated virus (LAV) is morphologically similar to animal lentiviruses, such as equine infectious anemia and visna viruses. This finding, together with the cross-reactivity of the core proteins of LAV with those of the equine infectious anemia virus and a similarity in genome structure and biological properties, allows LAV to be placed in the retroviral subfamily of Lentivirinae. Molecular data indicate a high degree of genetic variation of the virus, especially in the envelope gene, which have important implications for the origin of the virus (the T4 lymphotropism may be a recently acquired property) and for future immunization. Another problem is the role of viral infection in the induction of irreversible immunodeficiency. This syndrome occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV infection.
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PMID:Lymphadenopathy-associated virus: from molecular biology to pathogenicity. 299

The immunosuppressive effects of three herpesviruses--cytomegalovirus (CMV), Epstein-Barr virus (EBV), and herpes simplex virus (HSV)--were assessed in 29 renal transplant recipients treated with cyclosporine and prednisone. The ratios of Leu 3-positive ("helper-inducer") to Leu 2-positive ("suppressor-cytotoxic") T lymphocytes in peripheral blood were only moderately and transiently decreased during primary CMV infection, with or without concurrent reactivated EBV and HSV infections. This effect was due to an increase in absolute numbers of Leu 2-phenotypic and decrease in Leu 3-phenotypic T cells and was associated with symptomatic viral illness. Reactivated CMV infection alone or together with reactivated EBV and HSV infections resulted in less significant alterations in T-cell subsets than did primary CMV infection. Lymphocyte blastogenesis was not significantly altered during the herpesvirus infections. The data suggest that cyclosporine treatment inhibits the activation of suppressor cells and depression of cellular immune function that have been associated with herpesvirus infections in renal transplant recipients undergoing conventional immunotherapy.
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PMID:Effect of herpesvirus infections on T-lymphocyte subpopulations and blastogenic responses in renal transplant recipients receiving cyclosporine. 300 96

To determine whether major depressive disorder might be associated with serologic evidence for a chronic active Epstein-Barr virus infection, viral-specific antibodies were measured in two separate groups of depressed patients (N=43) and in 46 appropriately matched healthy volunteers. No evidence that depression affects cellular immunity to the point that a persistent Epstein-Barr virus carrier state becomes activated was found. There was also no evidence that depression results from an unrecognized chronic active Epstein-Barr virus infection. The authors conclude that the routine clinical determination of expensive commercial Epstein-Barr virus antibody profiles is not indicated in most patients with major depressive disorder in the absence of other signs of chronic active Epstein-Barr viral infection.
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PMID:Serum antibodies to Epstein-Barr virus in patients with major depressive disorder. 302 14

Various reports have indicated that infection of polymorphonuclear leukocytes (PMNL) with influenza virus causes depression of their metabolic and chemotactic responses, but the effect the PMNL has on the life cycle of influenza virus has not been well defined. The studies reported here were undertaken to determine whether influenza virus could replicate within PMNL. Virus-infected and uninfected PMNL were labeled with [35S]methionine and analyzed by gel electrophoresis and fluorography for detection of newly synthesized proteins. Both host- and virus-specific proteins were produced within PMNL. By using indirect immunofluorescence techniques combined with flow cytometry, the expression of newly synthesized viral antigens was detected in virus-infected PMNL. Plaque assays on supernatant fluid from infected PMNL showed that infectious progeny were not produced, indicating that influenza virus infection of PMNL is abortive.
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PMID:Synthesis of viral proteins in polymorphonuclear leukocytes infected with influenza A virus. 304 49

Myalgic Encephalomyelitis or post-viral fatigue syndrome is a common disorder, which has been known previously under a variety of different names, i.e., Iceland disease or Royal Free disease. It may occur in epidemics or sporadically. The cause is unknown, with patients complaining of exhaustion, fatigue, muscle aches and pains, and invariable psychiatric symptoms such as emotional lability, poor memory/concentration, and depression. Present-day research points to the cause as a metabolic disorder secondary to persistent viral infection.
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PMID:Postviral fatigue syndrome. 306 94


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