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 cell mediated immune (CMI) response was studied by E-rosette formation in vitro and delayed type hypersensitivity (DTH) skin reaction in buffalo calves vaccinated with monovalent type 0 as well as with a polyvalent foot-and-mouth disease vaccine. Up to 35 days post-vaccination there was a significant increase (P less than 0.05) in the number of T-lymphocytes in both animal groups. Thereafter, the number of lymphocytes decreased. Delayed type hypersensitivity (DTH) skin reaction was characterized by a significant increase in skin thickness; histology showed mononuclear infiltration and perivascular cuffing.
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PMID:Cell mediated immune response following foot-and-mouth disease vaccination in buffalo calves. 286 64

Cattle persistently infected with foot-and-mouth disease virus were treated with dexamethasone to suppress the immune system in an attempt to influence the level of virus recovery from oesophageal pharyngeal (probang) samples. Twelve carrier cattle were assigned to one of three groups: control; 0.1 mg/kg dexamethasone; and 0.5 mg/kg dexamethasone. Groups 2 and 3 were injected intramuscularly three times weekly for 3 weeks with dexamethasone between days 33 and 56 post-infection with foot-and-mouth disease virus (FMDV). Cattle in both groups developed a leucocytosis, neutrophilia and lymphopenia. The secretory IgA response to FMDV infection was inhibited following, but not during, dexamethasone treatment between days 70 and 98 post-infection (P < 0.05). FMDV recovery from probang samples was reduced between days 40 and 64 post-infection (P < 0.05) during treatment with either 0.1 or 0.5 mg/kg dexamethasone. Following cessation of dosing with dexamethasone virus recovery returned to control levels. These observations suggest dexamethasone inhibits shedding of FMDV in a reversible manner which may be related to its immunosuppressive, anti-inflammatory or physiological actions.
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PMID:Dexamethasone inhibits virus production and the secretory IgA response in oesophageal-pharyngeal fluid in cattle persistently infected with foot-and-mouth disease virus. 912 95

Pigs were vaccinated with the emergency inactivated foot-and-mouth disease virus (FMDV) vaccine--water-in-oil-in-water emulsion with Montanide ISA206--known to protect after 3-5 days. Peripheral blood leukocyte (PBL) sub-populations did not differ between vaccinates and controls post-vaccination. There was neither lymphopenia nor inflammatory reaction. FMDV-specific antibody and T lymphocyte activity developed in the vaccinates. Virus-induced Th1-like cytokine protein and mRNA (IFNgamma and IL-2) were identified, particularly IFNgamma. Th2-like cytokine protein and mRNA (IL-4 and IL-6) were also induced in an FMDV-specific manner. IL-10 was induced by both virus and mock antigen. The current emergency FMDV vaccine induces a diverse immune defence network--innate, and both Th1-like and Th2-like responses--without adverse reactions such as lymphopenia or inflammatory responses.
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PMID:Immune response characteristics following emergency vaccination of pigs against foot-and-mouth disease. 1562 Apr 77

African buffalo (Syncerus caffer) play an important role in the maintenance of the SAT types of foot-and-mouth disease (FMD) in southern Africa. These long-term carriers mostly become sub-clinically infected, maintaining the disease and posing a threat to other susceptible wildlife and domestic species. During an unrelated bovine tuberculosis experiment using captive buffalo in the Kruger National Park (KNP), an outbreak of SAT-1 occurred and was further investigated. The clinical signs were recorded and all animals demonstrated significant weight loss and lymphopenia that lasted 100 days. In addition, the mean cell volume and mean cell haemoglobin values were significantly higher than before the outbreak started. Virus was isolated from several buffalo over a period of 167 days post infection and the molecular clock estimated to be 3 x 10(-5) nucleotide substitutions per site per day. Seven amino acid changes occurred of which four occurred in hypervariable regions previously described for SAT-1. The genetic relationship of the outbreak virus was compared to buffalo viruses previously obtained from the KNP but the phylogeny was largely unresolved, therefore the relationship of this outbreak strain to others isolated from the KNP remains unclear.
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PMID:Characterisation of a SAT-1 outbreak of foot-and-mouth disease in captive African buffalo (Syncerus caffer): clinical symptoms, genetic characterisation and phylogenetic comparison of outbreak isolates. 1719 52

Viruses have evolved multiple mechanisms to evade the innate immune response, particularly the actions of interferons (IFNs). We have previously reported that exposure of dendritic cells (DCs) to foot-and-mouth disease virus (FMDV) in vitro yields no infection and induces a strong type I IFN (IFN-alpha and IFN-beta) response, indicating that DCs may play a critical role in the innate response to the virus. In vivo, FMDV induces lymphopenia and reduced T-cell proliferative responses to mitogen, viral effects that may contribute to evasion of early immune responses. In this study we analyzed the in vivo effects of FMDV infection on the IFN-alpha response of two populations of dendritic cells. During the acute phase of infection of swine, production of IFN-alpha from monocyte-derived DCs (MoDCs) and skin-derived DCs (skin DCs) is inhibited. This effect occurs concurrently with rising viral titers in the blood; however, these cells are not productively infected. Interestingly, there are no changes in the capability of these DCs to take up particles and process antigens, indicating that antigen-presenting cell function is normal. These data indicate that inhibition of the IFN-alpha response of dendritic cell populations from blood and skin by FMDV enhances viral pathogenesis in infected animals.
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PMID:Interferon-alpha production by swine dendritic cells is inhibited during acute infection with foot-and-mouth disease virus. 1835 24