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)

An immunohistochemical and histopathological study using the ABC technique was carried out to examine time-sequential virus spread in the central nervous system (CNS) of mice after inoculation with the CVS strain of fixed rabies virus by different routes; intracerebral (ic), intraocular (io), intranasal (in), intramuscular (im) and subcutaneous (sc). Only the ic and io inoculations caused fatal infections, so that detailed analysis was conducted on mice inoculated by these two routes. In ic-inoculated mice, viral antigens were detected mainly in neurons in the cerebral cortex and in the pyramidal cells and granular cells of the hippocampus. After io inoculation, viral antigen was first detected in the trigeminal nerve ganglia, following which it spreads to the cerebral cortex and cerebellum. In the hippocampus only a few cells were viral antigen-positive at the early stage after io inoculation. There were no inflammatory lesions or Negri bodies in the CNS of mice infected by either route. This suggests that clinical signs such as ataxia or depression leading to death may be due to the direct effect of the virus on the functions of neural cells, but not to inflammatory reactions. The ABC method will be useful for the early diagnosis of suspected patients or animals to have the disease when conventional histopathological and immunofluorescent antibody techniques can not detect lesions or viral antigens.
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PMID:Immunohistochemical and histopathological study of experimental rabies infection in mice. 164 65

The mechanism and cellular targets of mononuclear cell depletion were investigated in strains of mice susceptible or resistant to lethal infection with a virulent street rabies virus (SRV). Significant depletion was evident in the thymus of all infected animals at approximately 5 days postinfection and subsequently involved the spleen and lymph nodes in mice developing clinical signs of rabies. Immunofluorescent analyses of lymphocyte subsets in depleted spleens revealed that cell losses were non-selective since the relative proportions of K+, Thy-1+, Lyt-1+, and Lyt-2+ cells remained unchanged. Diminished expression of I-A membrane glycoproteins on spleen lymphocytes was noted, however, perhaps reflecting reduced availability of I-A-inducing lymphokines. Adrenal hormone toxicity was identified as the cause of mononuclear cell depletion in that mice adrenalectomized before SRV infection showed no evidence of lymphoid depletion. The failure of adrenalectomy to alter anti-rabies antibody responses or SRV lethality also indicates that involution of the lymphoid system is a consequence and not a cause of genetically controlled host susceptibility to SRV. The mechanism of adrenal gland stimulation in rabies-infected mice appears to involve a virus-induced dysfunction in the pituitary gland rather than a stress response to paralysis-induced starvation, based on results of kinetic studies on weight loss, appetite depression, and paralysis in these animals and previous reports of pituitary infection during rabies disease. The relationship of these observations to current theories on rabies virus pathogenicity is discussed.
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PMID:Murine susceptibility to street rabies virus is unrelated to induction of host lymphoid depletion. 232 81

Studies of rabies virus in several animal models consistently showed hypothalamic infection, hypophyseal infection, dramatic growth impairment (in the form of failure to thrive), wasting syndrome, and immune depletion. Rabies virus infection was studied through routine monoclonal antinucleocapsid antibody immunofluorescence and through a peroxidase-antiperoxidase immunoperoxidase method. The latter was modified to detect the in situ production of growth hormone by uninfected and rabies virus-infected adeno-a-pituicytes (with confirmation of the results both in vivo and in vitro). Infection with rabies virus made the specialized pituicytes produce less growth hormone. Growth before rabies virus infection and its reduction due to infection were investigated in a linear regression model. The fit was statistically significant (P less than .05) in all species studied: mouse, rat, rabbit, cow, and cat. Immune depression was studied in terms of alterations in the immunotopography of the thymus and also the specific T- and B-cell homing areas of the spleen (although spleen data are not presented here). On the basis of these results and a thorough review of wasting syndromes encountered in other diseases, a primary failure to thrive and an ensuing wasting syndrome were described and characterized for rabies, and their origin was assigned to a dysfunction of the hypophyseal/hypothalamic/thymic axis associated with at least (but not necessarily only) one of the centrally controlled growth hormones.
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PMID:Failure to thrive, wasting syndrome, and immunodeficiency in rabies: a hypophyseal/hypothalamic/thymic axis effect of rabies virus. 320 86

Twenty samples from cases of rabies in humans and domestic animals diagnosed in Venezuela between 1990 and 1994 and one sample from a vampire bat collected in 1976 were characterized by reactivity to monoclonal antibodies against the viral nucleoprotein and by patterns of nucleotide substitution in the nucleoprotein gene. Three antigenic variants were found: 1, 3, and 5. Antigenic variant 1 included all samples from dogs and humans infected by contact with rabid dogs. Unique substitutions permitted identification of two separate outbreaks of dog rabies in the Maracaibo Depression and Los Llanos region and in the Andean region of Venezuela. Samples from the vampire bat and two head of cattle were characterized as antigenic variant 3 and showed a nucleotide sequence homology of 96 to 98% to each other and to samples of vampire bat-associated rabies throughout Latin America. Ten of the remaining 12 samples were characterized as antigenic variant 5. Genetic studies indicated that 11 of these samples formed a highly homologous and distinctive group but were closely related to samples of vampire bat-associated rabies. The 12th sample of variant 5 (from a cat) showed only 78 to 80% genetic homology to samples of rabies associated with vampire bats. The application of antigenic and genetic typing to rabies surveillance in Latin America is essential to improve control programs. Recognition of the source of outbreaks of dog rabies and identification of wildlife species maintaining sylvatic cycles of rabies transmission permit better utilization of public health resources.
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PMID:Genetic characterization of rabies field isolates from Venezuela. 873 18

It is known that rabies virus can suppress the host immune system. In this study we demonstrate a depression of cell-mediated immunity in mice, peripherally infected with Thai street rabies virus. The cell-mediated cytolysis of spleen cells from mice increased transiently on day 5 after infection and declined rapidly thereafter until death. The proliferation of spleen cells stimulated with a T-cell mitogen such as phytohemagglutinin or concanavalin A, was significantly suppressed during the course of infection. There was also a marked suppression of IL-2 secretion in parallel with a decrease of the T-cell proliferative response to mitogen. The suppression of T-cell proliferation was not restored by treatment with a calcium ionophore (A 23187) or phorbol 12-myristate-13 acetate (PMA).
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PMID:Cell-mediated immunosuppression in mice by street rabies virus not restored by calcium ionophore or PMA. 943 44

To investigate the involvement of various cellular and humoral aspects of immunity in the clearance of rabies virus from the central nervous system, (CNS), we studied the development of clinical signs and virus clearance from the CNS in knockout mice lacking either B and T cells, CD8+ cytotoxic T cells, B cells, alpha/beta interferon (IFN-alpha/beta) receptors, IFN-gamma receptors, or complement components C3 and C4. Following intranasal infection with the attenuated rabies virus CVS-F3, normal adult mice of different genetic backgrounds developed a transient disease characterized by loss of body weight and appetite depression which peaked at 13 days postinfection (p.i.). While these animals had completely recovered by day 21 p.i., mice lacking either B and T cells or B cells alone developed a progressive disease and succumbed to infection. Mice lacking either CD8+ T cells, IFN receptors, or complement components C3 and C4 showed no significant differences in the development of clinical signs by comparison with intact counterparts having the same genetic background. However, while infectious virus and viral RNA could be detected in normal control mice only until day 8 p.i., in all of the gene knockout mice studied except those lacking C3 and C4, virus infection persisted through day 21 p.i. Analysis of rabies virus-specific antibody production together with histological assessment of brain inflammation in infected animals revealed that clearance of CVS-F3 by 21 days p.i. correlated with both a strong inflammatory response in the CNS early in the infection (day 8 p.i.), and the rapid (day 10 p.i.) production of significant levels of virus-neutralizing antibody (VNA). These studies confirm that rabies VNA is an absolute requirement for clearance of an established rabies virus infection. However, for the latter to occur in a timely fashion, collaboration between VNA and inflammatory mechanisms is necessary.
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PMID:Collaboration of antibody and inflammation in clearance of rabies virus from the central nervous system. 955 53

Four of approximately 15 dry cows introduced on a 10-acre fescue-clover-orchard grass-Dallis grass pasture in East Tennessee became recumbent. Clinical findings included depression, muscle tremors, increased heart and respiratory rates, hypocalcemia, hypomagnesemia, hyperkalemia, azotemia, and elevated creatinine phosphokinase. Three cows recovered; 1 died. Differential diagnoses considered were hypocalcemia, hypomagnesemia, rabies and toxicoses from Amaranthus retroflexus (pigweed), Quercus spp (oak), Cassia spp (senna) oxalate (Aspergillus niger or flavus), mycotoxicosis, lead, arsenic or insecticides. Pigweed toxicosis was confirmed based on clinical and postmortem findings, partially ingested pigweed in the pasture, and ruling out other possible causes. Several factors probably contributed to this incident: since the cattle were newly introduced to the pasture, the cattle may have been attracted to the pigweed in the new pasture and became addicted to it; their rumen microflora had little time to acclimate to the pigweed; and dry weather produced poor forage quality thus forcing the cows to eat the pigweed.
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PMID:Pigweed (Amaranthus retroflexus) toxicosis in cattle. 968 7

Previously, we demonstrated a depression of cell-mediated immunity in mice by street rabies virus infection. In the present study, we investigated several events during the course of infection and looked for alterations in the host lymphoid cells for evidence of apoptosis. Total cellular RNA was extracted from muscle tissues at the inoculation site of peripherally infected mice at different intervals after infection. Rabies virus mRNA was monitored by reverse transcription-PCR. The length of virus localization at the site of exposure in the muscle was as long as 5 days post-inoculation before the virus entered the central nervous system. At this inoculation site, the virus disappeared transiently between days 7 and 9 after infection but then was restored thereafter until death. Annexin V-fluorescein isothiocyanate staining of splenocytes and thymocytes from mice revealed apoptotic changes in these cells with a marked increase after day 6 of infection. Rabies virus antigen in the brain became detectable 6 days after infection; this occurred parallel to the appearance of apoptosis in the lymphoid cells. There was atrophy of the spleen and thymus, with no evidence of infection. Our results suggest that the interaction between the rabies virus and infected neurons triggers the process of lymphoid cell apoptosis, which reflects the defective operation of the immune system.
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PMID:Immunosuppression in rabies virus infection mediated by lymphocyte apoptosis. 1168 83

Rabies and associated risk factors in dogs, cats and cattle (n = 3,454) in southern Thailand during 1994-2008 were evaluated by using a mixed-effect logistic regression model. Overall prevalence was 48%. In dogs, odds of being rabid were 1.7 times higher in unvaccinated dogs than in vaccinated dogs and two times higher in dogs with bite history than in dogs with no known bite history. Similarly, aggressive dogs were more likely to be rabid than non-aggressive dogs. In cattle, aggression, pharyngeal paralysis, hyperactivity, and depression were clinical signs associated with being rabid. Annual fluctuations of the species-specific prevalence of rabies is suggestive of a positive correlation between canine and either feline (r = 0.60, P = 0.05) or bovine rabies (r = 0.78, P = 0.004). Insufficient vaccination coverage led to maintenance of rabies, which could be easily controlled by increased vaccine coverage and public education.
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PMID:Epidemiologic trends of rabies in domestic animals in southern Thailand, 1994-2008. 2173 39

The generation of purposive movement by mammals involves coordinated activity in the corticospinal and corticostriatal systems, which are involved in different aspects of motor control. In the motor cortex, corticospinal and corticostriatal neurons are closely intermingled, raising the question of whether and how information flows intracortically within and across these two channels. To explore this, we developed an optogenetic technique based on retrograde transfection of neurons with deletion-mutant rabies virus encoding channelrhodopsin-2, and used this in conjunction with retrograde anatomical labeling to stimulate and record from identified projection neurons in mouse motor cortex. We also used paired recordings to measure unitary connections. Both corticospinal and callosally projecting corticostriatal neurons in layer 5B formed within-class (recurrent) connections, with higher connection probability among corticostriatal than among corticospinal neurons. In contrast, across-class connectivity was extraordinarily asymmetric, essentially unidirectional from corticostriatal to corticospinal. Corticostriatal neurons in layer 5A and corticocortical neurons (callosal projection neurons similar to corticostriatal neurons) similarly received a paucity of corticospinal input. Connections involving presynaptic corticostriatal neurons had greater synaptic depression, and those involving postsynaptic corticospinal neurons had faster decaying EPSPs. Consequently, the three connections displayed a diversity of dynamic properties reflecting the different combinations of presynaptic and postsynaptic projection neurons. Collectively, these findings delineate a four-way specialized excitatory microcircuit formed by corticospinal and corticostriatal neurons. The "rectifying" corticostriatal-to-corticospinal connectivity implies a hierarchical organization and functional compartmentalization of corticospinal activity via unidirectional signaling from higher-order (corticostriatal) to lower-order (corticospinal) output neurons.
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PMID:Hierarchical connectivity and connection-specific dynamics in the corticospinal-corticostriatal microcircuit in mouse motor cortex. 3133 24


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