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)

To assess whether an virus-specific immune defect may be associated with multiple sclerosis (MS), we have examined the ability to generate measles virus-and influenza virus-specific cytotoxic T cells (CTL) in patients with MS, normal individuals, and other disease controls (ODC). The mean (+/- SEM) measles virus-specific CTL response for normal individuals and ODC was 26.9 +/- 2.9% (N = 17) and 26.7 +/- 2.8% (N = 13) specific lysis, respectively. In contrast, the capacity of MS patients to generate measles virus-specific CTL was markedly diminished. Peripheral blood lymphocytes from MS patients stimulated with measles virus lysed their measles virus-infected autologous B cell line at a group mean level of 6.0 +/- 1.4% (N = 16) specific lysis. MS patients had significantly lower measles virus-specific CTL responses than normal individuals (p less than 0.00001) or ODC (p less than 0.0001). Importantly, this lowered response did not reflect a generalized depressed cytolytic activity of MS patients, since influenza virus-specific CTL and NK activity from these patients were comparable to normals and ODC. Thus, in MS there is a significant depression of measles virus-specific CTL which suggests that this virus-specific immune dysfunction may play a role in the pathogenesis of this disorder.
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PMID:Impaired measles virus-specific cytotoxic T cell responses in multiple sclerosis. 241 41

The effect of immobilization stress on the course of various forms of influenza infection has been investigated. Influenza was produced in 10-14-week-old inbred mice by intranasal infection with pathogenic influenza virus strain A/PR/8/34 (H1N1) at different doses. Immobilization for 6 hr resulted in the appearance of virus-inhibiting activity in the serum of mice. This activity suppressed the reproduction of test-virus in tissue culture, it was resistant to acid pH 2.0 treatment and to heating at 56 degrees C. However, the high level of virus-inhibiting activity failed to protect the animals from subsequent development of lethal influenza infection. Immobilization stress caused a transient depression of virus induced interferon (IFN) production, as revealed by the use of virus inducer at early intervals after stress. Contemporarily, the stress could aggravate the course of virus infection promoting its transition from non-lethal form into a lethal one and virus penetration into brain.
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PMID:Experimental influenza infection: influence of stress. 244 85

Pathological consequences of a severe outbreak of swine influenza (H1N1 virus) in the non immune sow at the beginning of pregnancy, under natural conditions. A sudden acute outbreak of fever, depression, anorexia and coughing in a group of nulliparous sows from a herd that was currently under epidemiological investigation lead to build a particular disposal of observation. The clinical signs were daily recorded including rectal temperature. Blood was taken from the sows at the beginning of the troubles and 3 weeks later for the detection of Aujesky's disease, coronavirus TGE-like, Influenza viruses A/H1N1 and A/H3N2 and Mycoplasma hyopneumoniae. Viral detection was attempted from nasal swabs and aborted fetuses during the acute phase. The clinical study showed fever reaching near 41 degrees C on most of the pigs and lasting usually from 2 to 5 days. The diagnosis of Influenza (virus swine H1N1) was established both on serology (massive seroconversion) and on the detection of the virus from the nasal swabs and from an aborted fetus. The control of the lungs of sows "not in pig" and culled showed extended lesions of bronchopneumonia and Pasteurella multocida was found. The technical consequences of this severe outbreak of Influenza on reproduction were mainly important at the beginning of pregnancy. Over 13 sows inseminated less than 1 week before the outbreak, only 3 farrowed (respectively 5.5 and 12 piglets); 7 returned to oestrus and 3 "not a pig" at 21 days (echotomography) did not show signs of heat and were culled. Over 8 pregnant sows (1 month of pregnancy), 6 farrowed normal litters and total embryonic resorption occurred in 2 sows. Over 18 pregnant sows (more than 45 days gestation) one aborted.
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PMID:[Pathologic consequences of a severe influenza outbreak (swine virus A/H1N1) under natural conditions in the non-immune sow at the beginning of pregnancy]. 255 Jan 69

The three-dimensional structure of human rhinovirus 14 has a deep surface depression or "canyon" encircling each of the twelve fivefold vertices. The canyon's surface is inaccessible to the broad antigen binding region of antibodies, permitting conservation of residues that might be required for host cell receptor recognition without danger of attack by the host's immune system. In contrast, the exposed surface features, where neutralizing antibodies are known to bind, change rapidly under pressure from the host's immune system. It was, therefore, hypothesized that this depression was the site of receptor attachment. Similar, but smaller, depressions had been observed previously on both the hemagglutinin and neuraminidase spikes of influenza virus. These have also been shown to be the site of host cell interaction. Although support for the canyon hypothesis was only circumstantial in the first place, there are now extensive confirmatory data. These include site-specific mutations of residues in the canyon and conformational changes induced in the canyon by the binding of small organic molecules, all of which alter receptor attachment. The strategy used in human rhinovirus 14 to protect the viral receptor attachment site from immune surveillance may be utilized not only in other picornaviruses but also in many other types of viruses including human immunodeficiency virus.
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PMID:The canyon hypothesis. 256 Sep 13

The three-dimensional structure of human rhinovirus 14 has a deep surface depression or "canyon" encircling each of the twelve 5-fold vertices. The canyon's surface is inaccessible to the broad antigen binding region of antibodies, permitting conservation of residues that might be required for host cell receptor recognition without danger of attack by the host's immune system. In contrast, the exposed surface features, where neutralizing antibodies are known to bind, change rapidly under pressure from the host's immune system. It was, therefore, hypothesized that this depression was the site of receptor attachment. Similar, but smaller, depressions had been observed previously on both the hemagglutinin and neuraminidase spikes of influenza virus. These have also been shown to be the site of host cell interaction. Although support for the canyon hypothesis was only circumstantial in the first place, there are now extensive confirmatory data. These include site-specific mutations of residues in the canyon and conformational changes induced in the canyon by the binding of small organic molecules, all of which alter receptor attachment. The strategy used in human rhinovirus 14 to protect the viral receptor attachment site from immune surveillance may be utilized not only in other picornaviruses but also in many other types of viruses including human immunodeficiency virus.
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PMID:The canyon hypothesis. Hiding the host cell receptor attachment site on a viral surface from immune surveillance. 267 Sep 20

Infection of polymorphonuclear leukocytes (PMNL) with influenza virus causes depression of PMNL metabolic and bactericidal activities. The studies reported here were undertaken to determine whether the hemagglutinin (HA) glycoprotein of influenza virus mediates this depression. PMNL were incubated with purified HA and the oxidative responses to exogenous stimuli were measured. The results indicate that HA, in either liposomes or protein aggregates referred to as rosettes, depressed PMNL oxidative responses. Depression was observed within 2 min of initial interaction of HA with PMNL and lasted more than 2 h. The membrane fusion activity of HA requires proteolytic cleavage of the HA, whereas the receptor binding activity does not. There was no difference in the ability of virions with cleaved or uncleaved HA to depress PMNL responses suggesting that the fusion event is not required for PMNL dysfunction. Inasmuch as the HA glycoprotein binds to sialic acid-containing receptors on the surface of the PMNL, we tested whether other sialic acid-specific binding proteins can mediate the reduction of PMNL responses. Sialic acid-specific lectins from Limulus polyphemus or Limax flavus were incubated with PMNL before measuring their responses to secondary stimulus. Depression was observed upon incubation with the lectins similar to that seen upon incubation with the HA or influenza virus. These results suggest that attachment of influenza virus to sialic acid-containing receptors is responsible at least in part, for suppressing PMNL oxidative responses.
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PMID:Depression of polymorphonuclear leukocyte functions by purified influenza virus hemagglutinin and sialic acid-binding lectins. 272 34

The effect of various strains of influenza virus on polymorphonuclear leucocyte (PMNL) function were studied by chemiluminescence (CL) and bacterial killing assays. All virus strains induced PMNL CL and peak CL correlated with haemagglutination (HA) but not neuraminidase (NA) activity of virus pools. Heat-treatment of virus pools generally had little effect on HA activity or ability to generate a PMN CL response but almost completely destroyed NA activity. Exposure of PMNL to each of the six virus strains resulted in loss of surface-associated sialic acid and a marked depression in both zymosan-induced PMNL CL and PMNL bactericidal capacity. However, there was no correlation between the degree of PMNL functional impairment and virus NA activity and, furthermore, heat treatment of virus pools removed NA activity but generally had little effect on their ability to reduce PMNL function. NA does not appear to play a primary role in impairment of PMNL function by influenza virus.
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PMID:Effect of influenza A on phagocytic cell function. 274 89

Twenty-two patients with Stages Ia to IVa cutaneous T cell lymphoma were entered into a controlled trial of interferon alfa-2a (Roferon-A). Patients initially received either 3 million IU interferon alfa-2a, or their dosage was escalated to 36 million IU intramuscularly daily for a 10-week induction period. At the end of induction, 14/22 (64%) of patients had an objective antitumor response: three patients had a complete response, ten patients had a partial response (greater than or equal to 50% resolution of clinical disease), and one patient had a minor response. Responders included those with Stages Ia to IVa cutaneous T cell lymphoma, and remissions have lasted at least 4 to 27.5 months. Three patients progressed from a partial to complete response with further treatment, for an overall complete response rate of 27%. Acute flu-like side effects were generally minor and transient. Malaise/fatigue, depression, anorexia, and weight loss were common chronic dose-related side effects and the most frequent reasons for dose reduction or discontinuation of drug. Leukopenia was the most common laboratory side effect and was also dose-related. Recombinant human leukocyte interferon alfa-2a is an effective and well-tolerated single-agent therapy for early and advanced cutaneous T cell lymphoma.
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PMID:Interferon alfa-2a in the treatment of cutaneous T cell lymphoma. 278 39

When polymorphonuclear leukocytes (PMN) are exposed to most harvests of influenza A virus (depressing virus, DV) for 20 min, chemotactic, secretory, and oxidative functions are depressed upon subsequent exposure to soluble or particulate stimuli. Other harvests of influenza A virus (non-DV) do not alter these activities. The DV-induced changes in multiple functions suggest the virus may interfere with steps involved in PMN activation. Because some of these steps may be regulated by protein phosphorylation, we examined the effect of non-DV and DV on cellular protein phosphorylation. PMN loaded with 32P-labeled inorganic orthophosphate were exposed to non-DV, DV, or buffer for 30 min; cells were then treated with buffer, FMLP (10(-6) M), or PMA (100 ng/ml) for 30 s. Samples were sonicated and centrifuged; cytosolic and particulate fractions were analyzed by SDS-PAGE and autoradiography. Exposure of PMN to either non-DV or DV caused phosphorylation of several cell proteins. However, when DV-treated PMN were then stimulated with FMLP or PMA, further phosphorylation was inhibited compared to non-DV- or buffer-treated cells. This suggests that DV-induced depression of PMN end-stage functions may be due to changes in cell protein phosphorylation. DV could interfere with phosphorylation of PMN proteins by altering protein kinase activity. We therefore examined the influence of non-DV and DV on some parameters that could affect kinase function. PMN intracellular [Ca2+] was monitored by using the fluorescent Ca2+ indicator, Indo 1, and cAMP levels were measured by RIA. PMN treated with DV alone or DV plus FMLP had higher intracellular [CA2+] than PMN similarly treated with non-DV or buffer. Exposure of PMN to non-DV, DV, or buffer caused minimal changes in cAMP levels, and similar increases occurred in cAMP levels upon FMLP stimulation. To determine whether DV interferes with transmembrane signaling, the effect of influenza virus on PMN transmembrane potential was studied by using a fluorescent cyanine dye. Transmembrane potential changes were greater in PMN exposed to DV than to non-DV or buffer; however, subsequent stimulation with FMLP caused equivalent changes in transmembrane potential. Our data show that protein phosphorylation in PMN is induced by DV and non-DV infection; upon subsequent stimulation with FMLP or PMA, there is inhibited cellular phosphorylation only in PMN previously exposed to DV.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in cell protein phosphorylation in human neutrophils exposed to influenza A virus. A possible mechanism for depressed cellular end-stage functions. 283 42

Influenza viruses have been shown to decrease the ability of polymorphonuclear leukocytes (PMN) to respond to a variety of stimuli. This study was done to determine if viral neuraminidase was responsible for decreased PMN function. Treatment of human PMN with purified neuraminidases from influenza virus, Vibrio cholerae, or Clostridium perfringens did not significantly affect the ability of human PMN to respond to stimulation. Occasional virus preparations that lacked the ability to depress PMN function did not differ in neuraminidase activity from viruses capable of causing depression. These results demonstrate that neuraminidase activity is not the cause of influenza virus-induced PMN dysfunction.
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PMID:Neuraminidase activity is not the cause of influenza virus-induced neutrophil dysfunction. 286 60


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