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Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present data on 14 patients with chronic symptoms of disabling fatigue in association with serologic evidence of active Epstein-Barr virus (EBV) infection. Two thirds were women, and the average age at onset was 29.6 years. Forty-three percent were known to have had previous infectious mononucleosis, but the usual criteria for that diagnosis were not helpful with the present syndrome. Eighty-six percent had serologic evidence of cytomegalovirus (CMV) infection. Profound immunodeficiency was not present, but 71% had partial hypogammaglobulinemia, and minor abnormalities of T cell subsets were noted in six of seven patients studied. Fifty-seven percent achieved temporary serologic and symptomatic remission after an average duration of 33 months. Only one patient has a sustained remission. Comparison is made with other reported chronic, recurrent, and persistent EBV syndromes, and tentative diagnostic criteria for chronic mononucleosis syndrome are presented. Recently available EBV serologic techniques allow for identification of patients who have reactivated EBV infection, and this reactivation may be related to symptoms.
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PMID:Chronic mononucleosis syndrome. 609 68

Viral infections are often associated with immunodeficiency states. Although T lymphocytes have been thought to suppress the host's response, the precise etiology remains unclear. Therefore, we characterized T lymphocytes from six patients during both acute and convalescent phases of infectious mononucleosis (IM) with monoclonal antibodies (titer, 10(-5) to 10(-7) to antigens restricted to the TH2- helper (T4) and TH2 suppressor (T5) T cell subsets as well as to a common T cell antigen (T3) and HLA-D related Ia antigens. It was found that during acute infectious mononucleosis, there is both activation and increase of suppressor T cells (T5+, Ia+ phenotype). Fuctionally, the acute IM lymphocytes suppress autologous T cell proliferation to antigens as well as pokeweed mitogen driven B cell immunoglobulin production. In contrast, convalescence is associated with a return to normal of T cell subsets and immune function. These results demonstrate that viral infections can preferentially activate a specific T cell subset and suppress the overall human immune response.
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PMID:The cellular basis for viral-induced immunodeficiency: analysis by monoclonal antibodies. 625 Nov 32

A 6-year-old boy suffered from a severe lymphadenopathy, characterized histologically by a fulminant polyclonal immunoblast proliferation simulating malignant lymphoma with many immunoblasts resembling Reed-Sternberg cells. He had no history of infectious mononucleosis but Epstein-Barr virus (EBV) infection was evident from serological findings, and EBV-associated nuclear antigen (EBNA) was demonstrated in a high percentage of lymphocytes of blood and lymph nodes. An adequate humoral response to EBV ruled out the possibility of an X-linked recessive lymphoproliferative syndrome as the underlying cause of chronic EBV infection. A chromosomal defect in a subpopulation of lymphocytes was induced by interferon and might somehow be associated with a subtle immunodeficiency of our patient. After exacerbation of the disease chemotherapy was included in the treatment but the patient died 9 months after the onset of the disease. At autopsy the lymphoblastic cell proliferation had changed from that of immunoblasts to cells resembling the Burkitt's lymphoma cells. A change of the proliferating cell type was supported by means of cytochemical and immunological cell markers. The presence of EBV in these cells was demonstrated with the EBNA technique. It is concluded that our case may well support the hypothesis, that EBV may induce lymphoma-like polyclonal immunoblast proliferation in immunodeficient individuals, and that occasionally a monoclonal proliferation of the Burkitt's lymphoma type may supervene.
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PMID:Histological and immunopathological studies in a case of chronic Epstein-Barr virus infection terminating in a Burkitt-like lymphoma. 625 16

An unusual antibody response to the Epstein-Barr virus (EBV) has been noted in patients with ataxia-telangiectasia. Of a group of 16 such patients 8 were found to have antibodies in their serum to the EBV viral capsid antigen (VCA), and 4 of them also had antibodies to the EBV early antigen (EA); antibodies to the nuclear antigen (EBNA), however, were absent in 3 of the 8. The antibody pattern persisted for more than 2 years in the patients available for follow-up study. In comparison, of 24 patients with various other immunodeficiency syndromes 9 were found to have EBV-VCA antibodies in their serum, but none of the 9 had EA antibodies and 3 lacked EBNA antibodies. Two other groups of subjects, all of whom had EBV-VCA and EBNA antibodies in their serum late after an EBV infection, were also studied; 82 had infectious mononucleosis and 55 were healthy and had no such history. EA antibodies were detected in 45 of the first group during the acute phase of the illness but persisted in only 6 of the 68 who were followed up for more than 2 years, and they were detected in only 7 of the second group.All eight lymphoblastoid cell lines established from the peripheral blood of the four patients with ataxia-telangiectasia who are still available for follow-up study express EBV-VCA, whereas most similar cell lines established from normal individuals express only EBNA. In two of these patients cell-mediated immunity, as assessed from lymphocyte transformation induced by mitogens, was markedly decreased but autologous cell-mediated immune regression of EBV-induced transformation of B (bone-marrow-derived)-lymphocytes was normal. The percentage of T (thymus-derived)-helper cells was greatly decreased in two of the three patients in whom it was measured, and the percentage of T-suppressor cells was greatly increased in one of them, but the percentage of total T-lymphocytes was within normal limits in all three.The possible significance of these findings - in particular, the persistence of EA antibodies and the diminished restriction of expression of EA - in the late development of tumours after an EBV infection in patients with ataxia-telangiectasia deserves careful attention. Finally, the apparent correlation between immunoglobulin deficiency and poor or absent EBNA antibody response warrants further study.
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PMID:Epstein-Barr virus antibodies in patients with ataxia-telangiectasia and other immunodeficiency diseases. 627 57

Tissues from patients thought to have Epstein-Barr virus (EBV)-induced lymphoproliferative diseases were probed for EBV genomes using 2 independent hybridization techniques. Tissues from six patients with the X-linked lymphoproliferative syndrome, all five renal allograft recipients with immunoblastic sarcoma, and eight patients with diverse types of immunodeficiency and lymphoproliferative diseases such as fatal infectious mononucleosis or malignant lymphoma associated with antecedent immunodeficiency contained significant numbers of EBV genome equivalents per cell. The use of 2 hybridization probes is recommended to confirm the presence of EBV genomes. The finding of significant numbers of EBV genomes in tissues from patients with immunodeficiency suggests that EBV is the etiological agent of the associated lymphoproliferative diseases.
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PMID:Documentation of Epstein-Barr virus infection in immunodeficient patients with life-threatening lymphoproliferative diseases by Epstein-Barr virus complementary RNA/DNA and viral DNA/DNA hybridization. 627 68

Analyses of 100 subjects with the X-linked lymphoproliferative syndrome (XLP) in 25 kindreds revealed four major interrelated phenotypes: infectious mononucleosis, malignant B-cell lymphoma, aplastic anemia, and hypogammaglobulinemia. Eighty-one of the patients died. Two male subjects were asymptomatic but showed immunodeficiency to Epstein-Barr virus (EBV). Seventy-five subjects had the infectious mononucleosis phenotype and concurrently, 17 subjects of this group had aplastic anemia. All subjects with aplastic anemia died within a week. Aplastic anemia did not accompany hypogammaglobulinemia or malignant lymphoma phenotypes. Hypogammaglobulinemia had been detected before infectious mononucleosis in three subjects, after infectious mononucleosis in five subjects, and was not associated with infectious mononucleosis in 11 boys with hypogammaglobulinemia. In nine subjects infectious mononucleosis appeared to have evolved into malignant lymphoma; however, the majority of patients with malignant lymphoma showed no obvious antecedent infectious mononucleosis. One subject had infectious mononucleosis following recurrent malignant lymphoma. Twenty-six of 35 lymphomas were in the terminal ileum. Results of immunologic and virologic studies of 15 survivors revealed combined variable immunodeficiency and deficient antibody responses to EBV-specific antigens. Mothers of boys with XLP exhibited abnormally elevated titers of antibodies of EBV. Subjects of both sexes with phenotypes of XLP should be investigated for immunodeficiency to EBV. Persons with inherited or acquired immunodeficiency may be vulnerable to life-threatening EBV-induced diseases.
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PMID:Epstein-Barr virus-induced diseases in boys with the X-linked lymphoproliferative syndrome (XLP): update on studies of the registry. 628 85

The X-linked lymphoproliferative syndrome is characterized by immunodeficiency to Epstein-Barr virus (EBV) manifested by severe or fatal infectious mononucleosis and acquired immunodeficiency. We studied immune responses in six males of a well-characterized kindred with the X-linked lymphoproliferative syndrome. Two males were studied before and during acute fatal EBV infection. Both individuals demonstrated normal cellular and humoral immunity before EBV infection. During acute EBV infection, both individuals developed vigorous cytotoxic cellular responses against EBV-infected and -uninfected target cells. Anomalous killer and natural killer T cell activity was demonstrated against a variety of lymphoid cell lines, autologous fibroblasts and autologous hepatocytes. Effector cells responsible for anomalous killing reacted with a pan-T cell monoclonal antibody, and belonged to the OKT.8 T cell subset. Death in each case was caused by liver failure, but one patient developed extensive liver necrosis, whereas the other developed a massive infiltration of the liver with EBV-infected immunoblasts after aggressive immunosuppressive therapy. Immunological studies were performed on four males who had survived EBV infection years previously. They demonstrated global cellular immune defects with deficiencies of lymphocyte proliferative responses to mitogens and antigens, humoral immune deficiencies, abnormalities of regulatory T cell subsets and deficient natural killer cell activity. We propose that an aberrant immune response triggered by acute EBV infection results in unregulated anomalous killer and natural killer cell activity against EBV infected and uninfected cells. These studies suggest that global immune defects appearing in males with X-linked lymphoproliferative syndrome who survive EBV infection are epiphenomenon.
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PMID:X-linked lymphoproliferative syndrome. Natural history of the immunodeficiency. 630 53

The observation by Epstein and Barr (EB) of virus particles in Burkitt lymphoma cells in 1964 led 4 years later to the discovery that this virus was the long sought agent responsible for infectious mononucleosis. Pathophysiologically the EB virus specifically infects B lymphocytes of the immune system and induces perpetual multiplication of these cells if infection remains uncontrolled. The T lymphocytes, once sensitized against these virus infected cells, either kill them or suppress their continuous growth. During acute infectious mononucleosis, these stimulated T cells appear in the bloodstream as "atypical lymphocytes". If cell-mediated immunity is hampered by either congenital or acquired immunodeficiency the proliferative potential of EBV infected B lymphocytes may become uncontrolled and lead either to fulminant and lethal infectious mononucleosis or to polyclonal or monoclonal B cell proliferation. This later phenomenon appears to be the source of most of the lymphoma observed in transplant patients who are chronically immunosuppressed. Much remains to be understood of the mechanisms of EBV infections, which in some geographic areas lead to inapparent infections and in others to Burkitt lymphoma or nasopharyngeal carcinoma, while in temperate regions the clinical manifestations are those of infectious mononucleosis.
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PMID:[The spectrum of infections caused by the Epstein-Barr virus]. 631 Jul 35

This report deals with the case history of a 21/2-year old Turkish boy, who died from an overwhelming mononucleosis infectiosa. The parents, first cousins, lost already two sons and a daughter. According to the parents, the symptoms of these children resembled those of this boy. In the patient, described here, an acquired immunodeficiency was found, probably induced by the Epstein-Barr virus on the basis of a genetic susceptibility for this virus. The family history, the clinical picture, together with the serological, immunological - and histological examinations, pointed to the diagnosis of X-linked recessive lymfoproliferative syndrome (XLP), as described by Purtilo. The immunological findings resemble those of AIDS (acquired immunodeficiency syndrome).
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PMID:[X-linked lymphoproliferative syndrome]. 654 57

The X-linked lymphoproliferative syndrome may be the model of a EBV-induced immunodeficiency which may lead, in case of T-insufficiency, either to myeloid aplasia, or to a polyclonal proliferation of the malignant, infectious mononucleosis (MI) type or, if it becomes secondarily monoclonal, non-hodgkin lymphoma (LNH).
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PMID:[EB virus, immunodeficiency, bone marrow aplasia, malignant mononucleosis and sex-linked lymphoproliferative B syndrome (XLP)]. 660 79


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