Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Virus replication and subsequent viremia are clearly correlated with clinical disease in EIAV infected horses. Termination of viremia is the result of specific immune responses. Recurrences of viremia are associated with antigenic variation of neutralization-sensitive epitopes. Immunosuppression experiments indicate that the eventual control of EIAV and development of carriers is mediated by the immune system. Even though the immune response to EIAV has a protective effect, immune responses also cause some of the lesions. At least one part of the anemia, erythrocyte destruction, is caused by the immune response. Not all of the mechanisms of decreased erythropoiesis are known, but EIAV infection of monocyte/macrophages results in altered iron metabolism and functional iron deficiency. Viral antigen-antibody-C3 complexes cause glomerulitis and the combination of antigen-antibody reactions results in significant reductions in plasma C3. Lesions in the liver and other organs are infiltrations of lymphocytes and monocytes/macrophages in the interstitial areas and it is assumed that these lesions are initiated by specific immune responses to viral antigens. The observations on kinetics of EIAV infection, immune control by the horse, and immunopathologic basis of most of the lesions lead to the conclusion that mechanisms of lentivirus control and disease can be determined by study of EIAV.
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PMID:Immunopathogenesis of equine infectious anemia lentivirus disease. 217 27

A case of acute parvovirus B19 infection causing fever, anaemia, leukopenia, and red cell aplasia, in a patient with chronic rheumatoid arthritis is described. The patient had received low doses of corticosteroids for several years, and a small dose of methotrexate recently. There was no evidence of haemolytic anaemia, iron deficiency or drug toxicity. Recovery was associated with the development of antibodies against parvovirus B19, and clearance of viraemia as detected by the polymerase chain reaction. Possible mechanisms for the development of leukopenia are discussed, but there was no evidence for haemophagocytosis.
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PMID:Parvovirus infection causing red cell aplasia and leukopenia in rheumatoid arthritis. 818 36

During the postnatal period the developing brain is vulnerable to insults including nutrient insufficiency and infection that may lead to disrupted development and cognitive dysfunction. Since iron deficiency (ID) often presents with immunodeficiency, the objective of this study was to investigate peripheral viremia and inflammation as well as brain microglial phenotype and function when ID and respiratory infection occur simultaneously in a neonatal piglet model. On postnatal day 2 (PD 2) male and female piglets were assigned to one of four treatments and fed either control or ID milk replacer. On PD 8 half the pigs on each diet were inoculated with either vehicle or porcine reproductive and respiratory syndrome virus (PRRSV; P-129). Blood samples were collected prior to inoculation (PD 7) and repeated once weekly. Rectal temperature, feeding score, and sickness behavior were measured daily until PD 28. Hematocrit, hemoglobin, and serum iron were reduced by ID but not PRRSV infection. PRRSV-infected piglets displayed viremia by PD 14; however, those fed control diet had lower viral titer on PD 28, while circulating virus remained elevated in those fed an ID diet, suggesting that ID either impaired immune function necessary for viral clearance or increased viral replication. ID piglets infected with PRRSV displayed reduced sickness behavior compared to those fed control diet on PD 13-15 and 18-20. While ID piglet sickness behavior progressively worsened, piglets fed control diet displayed improved sickness score after PD 21. Microglia isolated from PRRSV piglets had increased MHCII expression and phagocytic activity ex vivo compared to uninfected piglets. ID did not alter microglial activation or phagocytic activity. Similarly, microglial cytokine expression was increased by PRRSV but unaffected by ID, in stark contrast to peripheral blood mononuclear cell (PBMC) cytokine expression, which was increased by infection and generally decreased by ID. Taken together, these data suggest that ID decreases peripheral immune function leading to increased viremia, but immune activity in the brain is protected from acute ID.
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PMID:Dietary Iron Deficiency Impaired Peripheral Immunity but Did Not Alter Brain Microglia in PRRSV-Infected Neonatal Piglets. 3077 59