Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of non-organ-specific autoantibodies, such as antibodies to vimentin, centriole, the midbody of chromatin and the Golgi apparatus, were detected in the sera of patients with infectious mononucleosis or nasopharyngeal carcinoma, by using an indirect immunofluorescence technique. There was no significant correlation between the titers of anti-Epstein-Barr virus antibodies and those of autoantibodies. Our findings suggest that the autoantibody production is antigen-driven.
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PMID:Anti-organelle and anti-cytoskeletal autoantibodies in the serum of Epstein-Barr virus-infected patients. 165 74

Sera from patients with rheumatoid arthritis (RA), patients with infectious mononucleosis (IM), and blood donors were tested by indirect immunofluorescence for the presence of antikeratin antibody (AKA), antibody to cytoskeletal intermediate filaments of prekeratin or vimentin type (AIFA) and antiperinuclear factor (APF). In 81.9% of the RA sera and 92.5% of the IM sera AIFA of IgM class was found at titres up to and in some cases exceeding 1/160. In blood donors the incidence of AIFA was 26%, at titres not exceeding 1/20. AKA and APF, always of IgG class, were found in 54.2% and 73.6% of rheumatoid sera. A weak correlation was found in RA between the incidence of AIFA and APF. AKA was not present in either IM or blood donor sera, and APF was found in only 2.5% and 3.2% of IM or blood donors respectively.
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PMID:Anti-intermediate filament antibodies, antikeratin antibody, and antiperinuclear factor in rheumatoid arthritis and infectious mononucleosis. 241 Dec 30

A murine monoclonal antibody (MAb) (15TD3) was found to recognize a unique filamentous structure in Epstein-Barr virus (EBV)-producing lymphoblastoid cell lines. By immunofluorescent morphology, in comparison with a control MAb to vimentin, the 15TD3 filamentous structure was judged to be associated with intermediate filaments of the cytoskeleton. Expression of the 15TD3 antigen and vimentin was induced simultaneously in some EBV genome-positive cell lines either by EBV superinfection or by 12-0-tetradecanoyl-1-phorbol-13-acetate (TPA) and n-butyrate treatment. The 15TD3 antigen was considered to be a restricted component of the EBV-induced early antigen (EA) complex. The 15TD3 antigen was expressed only in EBV genome-activated cells after either spontaneous EBV genome activation, EBV superinfection, or TPA and n-butyrate treatment. The expression of 15TD3 antigen paralleled the induction of EA in several models of induction of EBV antigens, and was detected only in EA+ cells which were stained with anti-EA+ human sera. The reactivity of 15TD3 MAb was blocked with anti-EA+ human serum, but not with anti-EA- serum. The synthesis of 15TD3 antigen was not inhibited with phosphonoacetic acid, was resistant to acetone fixation, and was sensitive to ethanol (or methanol) fixation. Human lymphoblastoid cells from patients with acute infectious mononucleosis were cloned for the production of antibodies which detected EBV-specific or -nonspecific epitopes on filamentous structures. Two human MAb were defined by two-color immunofluorescence to react to the 15TD3 determinants on intermediate filaments of EBV+ cells. This study supports the following views: that EBV genome activation induces a structure associated with intermediate filaments, and that antibodies against both the EBV-specific, intermediate filament-associated epitope and native intermediate filament epitopes are produced by some EBV-transformed lymphoblastoid cell lines from patients with infectious mononucleosis.
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PMID:Immune response to intermediate filament-associated, Epstein-Barr virus-induced early antigen. 243 3

Serum antibodies to cytoskeletal systems were measured by indirect immunofluorescence using human skin fibroblasts and HEp2 cells as substrate. Healthy adults had IgM antibodies to vimentin and cytokeratin at 60 times serum dilution. IgG concentration did not have a correlation with IgG anti-cytoskeletal system antibodies and IgM concentration correlated with anti-vimentin and anti-cytokeratin antibodies. In patients with adult T-cell leukemia (ATL), IgG antibody titer against actin and vimentin was increased in spite of a decreased IgG concentration. IgM antibodies to vimentin was decreased in its titer together with a decreased IgM concentration. Antibody titer to HTLV-1, leukemic cell counts in peripheral blood and disease type, acute or chronic, did not have correlations with anti-cytoskeletal system antibodies. A third of the patients with ATL showed negative anti-EBNA antibody, suggesting that the functional impairment in EBV-specific killer cells was present. In contrast, the patients with infectious mononucleosis showed increased serum IgM concentration and IgM anti-vimentin antibody titer. It was suggested that the autoantibodies to cytoskeletal systems associated with viral infection were mainly composed of IgG in ATL and of IgM in infectious mononucleosis.
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PMID:[Antibodies to cytoskeletal systems in patients with adult T-cell leukemia and infectious mononucleosis]. 281 Jul 84

A history of infectious mononucleosis (IM), symptomatic primary infection with the Epstein Barr virus, is associated with the development of autoimmune diseases and increases the risk to develop multiple sclerosis. Here, we hypothesized that immune activation during IM triggers autoreactive immune responses. Antibody responses towards cellular antigens using a HEp-2 based indirect immunofluorescence assay and native myelin oligodendrocyte glycoprotein (MOG) using a flow cytometry-based assay were determined in 35 patients with IM and in 23 control subjects. We detected frequent immunoglobulin M (IgM) reactivity to vimentin, a major constituent of the intermediate filament family of proteins, in IM patients (27/35; 77%) but rarely in control subjects (2/23; 9%). IgG autoantibodies binding to HEp-2 cells were absent in both groups. In contrast, IgG responses to native MOG, present in up to 40% of children with inflammatory demyelinating diseases of the central nervous system (CNS), were detectable in 7/35 (20%) patients with IM but not in control subjects. Normalization of anti-vimentin IgM levels to increased total IgM concentrations during IM resulted in loss of significant differences for anti-vimentin IgM titers. Anti-MOG specific IgG responses were still detectable in a subset of three out of 35 patients with IM (9%), even after normalization to increased total IgG levels. Vimentin-specific IgM and MOG-specific IgG responses decreased following clinical resolution of acute IM symptoms. We conclude from our data that MOG-specific memory B cells are activated in subset of patients with IM.
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PMID:Infectious Mononucleosis Triggers Generation of IgG Auto-Antibodies against Native Myelin Oligodendrocyte Glycoprotein. 2690 24

Serum antibodies to cytoskeletal systems were detected, using indirect immunofluorescence in patients with adult T-cell leukemia (ATL), healthy carriers of human T cell lymphotropic virus 1 (HTLV-1), patients with infectious mononucleosis and healthy adults. Healthy carriers of HTLV-1 had IgG antibodies to cytoskeletal systems as evidenced by an increased incidence of IgG antibodies to actin and vimentin. Decreased IgG antibody levels to Epstein-Barr virus nucleic acid (EBNA) were also evident. In patients with ATL, the titers of IgM antibodies to vimentin and cytokeratin showed a positive correlation with decreased serum levels of IgM, despite the fact that serum concentrations of IgM were significantly decreased in patients with ATL. The IgM antibody titer divided by the IgM concentration (the antibody ratio) was nigher than that of healthy carriers and healthy adults, suggesting that the IgM antibody response to cytoskeletal systems was preferentially preserved in these cases. There was also a suggestion of the presence of polyclonal as well as specific antibody responses to cytoskeletal systems in patients with infectious mononucleosis. As a result of these findings we suggest that there is some difference in the mechanisms responsible for the production of autoantibodies to cytoskeletal systems following HTLV-1 infection and Epstein-Barr virus infection.
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PMID:Serum Antibodies to Cytoskeletal Systems in Patients with Adult T-Cell Leukemia and Healthy HTLV-1 Carriers. 2746 71