Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The natural resistance of adult specific-pathogen-free cats to feline leukemia virus (FeLV) was abrogated by treatment with various doses of a synthetic corticosteroid, methylprednisolone acetate (MPA), prior to either oral-nasal or i.p. inoculation of FeLV. Persistent viremia was induced in 82% (18 of 22) of MPA-treated cats versus 11% (1 of 9) of age-matched control cats. MPA-treated FeLV-inoculated cats developed prolonged lymphopenia (2 to 8 weeks postinoculation) and a delayed antibody response to the feline oncornavirus-associated cell membrane antigen. The distribution of FeLV group specific antigen in tissues of MPA-treated, FeLV-inoculated cats suggested that corticosteroids enhanced susceptibility to FeLV by impairing early viral containment in the reticuloendothelial and lymphoid tissues.
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PMID:Influence of adrenal corticosteroids on the susceptibility of cats to feline leukemia virus infection. 22 25

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

In utero acquistion of protective levels of neutralizing antibody to canine distemper virus (CDV) was observed in four litters of colostrum-deprived gnotobiotic and specific-pathogen-free puppies. Pregnant bitches with high antibody titers passively transferred antibody to these pups transplacentally in average titers of 1:7 to 1:16 per litter. Maternally derived antibody protected neonatal pups from otherwise fatal infection with virulent CDV. Protection was associated with a transient lymphopenia and viremia and temporary suppression of lymphocyte responses to phytohemagglutinin-P.
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PMID:Influence of transplacentally acquired antibody on neonatal susceptibility to canine distemper virus in gnotobiotic dogs. 65 17

Six specific pathogen-free foals shown to be free of equine herpesvirus-1 and 4 (EHV-1 and -4) and lacking in maternally-derived antibodies were used to investigate the pathogenesis of EHV-1 in horses. Following primary intranasal inoculation with EHV-1 all foals showed signs of a mild, self-limiting upper respiratory tract infection. A leucopenia was observed, comprising both a lymphopenia and neutropenia. Virus was isolated from nasal mucus and buffy coat cells over several days during the clinical episode and after the animals became clinically normal. Notwithstanding the mildness of the clinical disease, virus was not eliminated completely and intravenous administration of dexamethasone resulted in reactivation of latent EHV-1 in animals which had received only a single dose of the virus. In a second infection given to four foals, 61 days after the primary inoculation, no clinical signs were observed, haematological changes were minimal and viraemia was absent.
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PMID:Pathogenesis of equine herpesvirus-1 in specific pathogen-free foals: primary and secondary infections and reactivation. 131 51

Diabetogenic Coxsackievirus B4 infection may trigger autoimmune islet loss in diabetes-susceptible mice, resulting in hyperglycemia in nearly 90% of the animals at 6-8 weeks postinfection (p.i.). To ascertain whether changes in lymphocyte repertoire following infection could predispose these animals to diabetes, alterations in their thymic, splenic, and peripheral lymphocytes were analyzed. Additionally, lymphocyte changes were correlated with the virus load in these tissues and with lymphocyte migration to the inflammatory pancreas. Splenic B lymphocytes more than doubled at 72 hr p.i. and then continuously decreased by 16% of the noninfected controls at 8 weeks p.i. T lymphocytes (CD4+ + CD8+) decreased by about 50% at 72 hr and then increased to the control level by 8 weeks p.i.; CD8+ subset continuously decreased by 40% of the control at 8 weeks, resulting in a 67% increase in CD4+/CD8+ ratio. Macrophages and CD5+ B subset increased at 72 hr and then dipped by 93% and 84%, respectively, at 8 weeks. In contrast, peripheral B lymphocytes increased by 74% and T lymphocytes decreased by 11% at 8 weeks p.i. Macrophages increased by twofold at 72 hr and then dipped slightly (6%) at 8 weeks, whereas CD5+ B subset increased by 245%. Most prominent thymic T lymphocyte alteration was reflected by about 150% increase in CD4- CD8- cells at 8 weeks p.i. The peak viremia occurred at 72 hr p.i., with highest and lowest virus in the spleen and thymus, respectively. The thymus cleared virus by 3 days, the other tissues by 7 days. Insulitis and acinar necrosis followed infection; infiltrating lymphocytes were mostly CD4+. Virus-induced abnormal lymphocyte maturation may contribute to the development of insulitis and hyperglycemia.
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PMID:Coxsackievirus B4 infection alters thymic, splenic, and peripheral lymphocyte repertoire preceding onset of hyperglycemia in mice. 133 27

A study was performed to examine the effect of viral inoculum size on the appearance of clinical signs in equine Getah virus (GV) infection by intramuscular inoculation with 10(1.3) to 10(6.3) TCID50 of the MI-110 strain in 6 experimental horses. When inoculated with more than 10(3.3) TCID50 of the virus, every horse developed pyrexia, edema in the hind legs, serous nasal discharge, lymphopenia and viremia in the relatively early stage of disease. On the other hand, enlargement of the submandibular lymph node was observed only in horses inoculated with 10(5.3) and 10(6.3) TCID50 of the virus, while typical eruptions were developed in every horse inoculated with 10(4.3) TCID50 or less. These results demonstrated that the appearance of clinical signs in equine GV infection was dependent on viral inoculum size. Besides, it was assumed to be rare chance that eruptions and enlargement of the submandibular lymph node were developed simultaneously in a horse.
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PMID:Effect of viral inoculum size on appearance of clinical signs in equine Getah virus infection. 166 Nov 74

Aerosol transmission in equine Getah virus (GV) infection was examined by intranasal inoculation with 10(3.0) to 10(7.0) TCID50 of the MI-110 strain in 7 experimental horses. The establishment of intranasal infection of GV was confirmed in all these horses by detecting serum neutralizing antibody against the MI-110 strain. Horses inoculated with more than 10(4.0) TCID50 of the virus manifested mild pyrexia, eruptions, serous nasal discharge, lymphopenia or monocytosis. Viremia ranging from 10(1.0) to 10(3.5) TCID50/0.2 ml occurred in horses inoculated with 10(5.0) TCID50, or more. Virus recovery from the nasal cavity was observed only in horses inoculated with 10(7.0) TCID50, and the viral titers recorded were 10(3.0) TICD50/ml or less. From these results, it is assumed that GV disseminated from the nasal cavity of naturally infected horses, except for intranasal infection with a lot of the virus, is probably very low in titer. So it seems to be rare that GV in natural cycles is spread from horse to horse by aerosol transmission.
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PMID:Intranasal infection of Getah virus in experimental horses. 166 Nov 75

An infectious, virulence-attenuated molecular clone of simian immunodeficiency virus (SIV), SIVMAC-1A11, was derived from an SIV isolate that causes fatal immunodeficiency in rhesus macaques. When inoculated intravenously in rhesus macaques, SIVMAC-1A11 induced transient viremia (1 to 6 weeks) without clinical disease and a persistent humoral antibody response. The antibodies were directed mainly against the viral envelope glycoproteins, as determined by immunoblots and virus neutralization. The potential of this virulence-attenuated virus to protect against intravenous challenge with a pathogenic SIVMAC strain was assessed. Five rhesus macaques were each given two intravenous inoculations with SIVMAC-1A11 7 months apart. Three of the five immunized monkeys and four naive control animals were then challenged with 100 to 1,000 100% animal infectious doses of pathogenic SIVMAC. All seven animals became persistently viremic following the challenge. Four of four unimmunized animals developed severe clinical signs of simian acquired immunodeficiency syndrome by 38 to 227 days after challenge and were euthanatized 91 to 260 days postchallenge. However, no signs of illness were seen in immunized monkeys until 267 to 304 days postchallenge, when two of three immunized animals developed mild thrombocytopenia and lymphopenia; one of these animals died with clinical signs of simian immunodeficiency disease at 445 days after challenge. The two SIVMAC-1A11-immunized monkeys that were not challenged were healthy and antibody positive 22 months after the initial immunization. Thus, although live SIVMAC-1A11 was immunogenic and did not induce any disease, it failed to protect rhesus macaques against infection with a moderately high dose of pathogenic virus. However, immunization prevented severe, early disease and prolonged the lives of monkeys subsequently infected with pathogenic SIV.
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PMID:Immunization with a live, attenuated simian immunodeficiency virus (SIV) prevents early disease but not infection in rhesus macaques challenged with pathogenic SIV. 216 91

Severe progressive immunodeficiency syndrome can be induced experimentally with a molecularly cloned isolate of feline leukemia virus (FeLV-FAIDS). The resultant disease syndrome is characterized by persistent viremia, lymphopenia, progressive weight loss, persistent diarrhea, enteropathy, and opportunistic infections. The onset of clinical immunodeficiency disease is prefigured by the replication of the FeLV-FAIDS variant virus in bone marrow and other tissues. The FeLV-FAIDS system can be used to evaluate antiviral agents which act on steps in the replication cycle which are conserved among retroviruses (e.g. reverse transcriptase, protease, assembly). The persistence and magnitude of viremia serves as a useful parameter in antiviral studies because it can be easily measured, presages the eventual development of immunodeficiency, and provides a convenient indicator of therapeutic efficacy either in preventing de novo FeLV infection or in reversing or ameliorating established infection. We describe here the evaluation of 2',3'-dideoxycytidine (ddC) against FeLV-FAIDS infection - both in vitro in cell culture assay systems and in vivo in cats administered ddC either via intravenous bolus dosage or via controlled release subcutaneous implants. We found that, although controlled release delivery of ddC inhibited de novo FeLV-FAIDS replication and delayed onset of viremia when therapy was discontinued (after 3 weeks), an equivalent incidence and level of viremia were established rapidly in both ddC-treated and control cats. The FeLV model, therefore, can be used to assess rapidly experimental single agent or combined antiviral therapies for persistent retrovirus infection and disease.
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PMID:Feline leukemia virus-induced immunodeficiency syndrome in cats as a model for evaluation of antiretroviral therapy. 254 Jan 9

The effect of two anti-inflammatory drugs on the development and persistence of clinical signs in cattle experimentally infected with bovine ephemeral fever (BEF) virus was investigated by their administration, either before or after the commencement of fever. A total of 16 cattle was given phenylbutazone sodium (PBZ). The drug prevented fever and other clinical signs in six cattle when given daily during the incubation period, and at 8-h intervals for 5 days when clinical disease might be expected. When treatment with PBZ was deferred until 2-4 h after the commencement of fever, the rectal temperature returned to normal within 4 h in four of six cattle and the development of other clinical signs was suppressed. Clinical signs of ephemeral fever occurred in four untreated cattle infected at the same time. Viraemia, the development of neutralizing antibodies (at 8-11 days), resistance to subsequent challenge with BEF virus, neutrophilia, lymphopenia and a rise in plasma fibrinogen occurred in all BEF-infected animals whether treated or untreated, despite different clinical appearances. The mean peak of plasma fibrinogen in the untreated cattle was 6.9 g l-1; 3.2 g l-1 when treated 2-4 h after fever developed and 3.8 g l-1 when treated from 18-h post-infection. BEF virus was isolated from leucocytes of each of the cattle, but the frequency of isolation was lower in the treated group. The results indicate that treatment with PBZ blocked the host response which produces the clinical signs and did not have an anti-viral effect. In a similar experiment, a long-acting anti-inflammatory drug, flunixin meglumine, failed to prevent BEF or to modify the clinical signs once they had developed, except for the rectal temperature which returned to normal within 2-4 h of the administration of the drug. The efficacy of this drug was not improved by increasing the dosage to two or three times the recommended level.
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PMID:The effect of anti-inflammatory agents on the clinical expression of bovine ephemeral fever. 270 92


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