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)

We describe a 14-year-old girl with fatal infectious mononucleosis with high fever, pancytopenia, and multiple skin ulcers due to Staphylococcus aureus. Immunological studies revealed low serum IgM, low natural killer (NK) activity, and high CD4/CD8 ratio. Her father had also low NK activity and high CD4/CD8 ratio. It is suggested that she had a dominantly inherited immunodeficiency predisposing to severe Epstein-Barr virus infection.
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PMID:Fatal infectious mononucleosis with staphylococcal pyoderma in a girl with hereditary immunological dysregulations. 261 6

We report on two patients with acute human immunodeficiency virus (HIV) infection, who developed an infectious mononucleosis-like clinical episode with thrombocytopenia and granulocytopenia. In both cases we detected the presence of IgG antigranulocyte antibodies and in one case the presence of IgG, IgM and IgA antiplatelet antibodies. The mechanisms of these cytopenias are discussed. The association between such autoimmune cytopenias and acute HIV infection has not been previously reported. We suggest testing for HIV seroconversion in patients with a seronegative infectious mononucleosis-like syndrome belonging to groups with a high risk for HIV infection.
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PMID:Autoimmune neutropenia and thrombocytopenia associated with development of antibodies to human immunodeficiency virus. 270 31

Epstein-Barr virus (EBV) is a ubiquitous transforming virus of the herpes group showing tropism for B lymphocytes. Primary infection in normal hosts results in a transient lymphoproliferative disorder, acute infectious mononucleosis (IM), that is restricted by cytotoxic and suppressive lymphocytes. However, in the immunodeficient host, EBV-induced lymphoproliferation may behave in a biologically malignant fashion. Patients with primary immunodeficiencies and those with immune incompetence resulting from suppressive therapy in allograft transplantation or infection with human immunodeficiency virus (HIV) have EBV-related illness ranging from fulminant mononucleosis and invasive polyclonal B cell hyperplasia to monoclonal B cell malignancies. While the direct link between EBV and malignant B cell proliferation in these patients has not been elucidated, the association has been increasingly recognized with improved techniques of viral detection. Clinical management can be guided by the location and extent of tumor, histologic features, and clonality. Regional and node-based polyclonal proliferations may respond to prompt reduction of immunosuppressive therapy and efforts to interrupt the replicative cycle with antiviral agents. Systemic cytotoxic therapy often leads to further immunosuppression and should be reserved for patients with progressive disease, advanced visceral involvement, and monoclonal lymphoid malignancies.
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PMID:Lymphoproliferative diseases in immunocompromised hosts: the role of Epstein-Barr virus. 282 Nov 99

Both oral and intravenous acyclovir administration for seven days in the early stages of infectious mononucleosis caused an inhibition of oropharyngeal Epstein-Barr virus (EBV) replication. Minimal effect on clinical symptoms was observed. Development of normal cellular and humoral EBV-specific immunity was seen in all patients. The combination of intravenous acyclovir and prednisolone treatment for 10 days in 11 patients with fulminant mononucleosis caused transient cessation of virus shedding in all patients. A dramatic clinical effect on pharyngeal symptoms and on fever was seen in nine of 11 patients within 72 hours. Treatment with chemotherapy or irradiation is recommended in EBV-associated B cell lymphomas seen in immunosuppressed, transplanted, and human immunodeficiency virus-I seropositive patients. No effect of acyclovir has been reported, but such therapy may be considered in the early stage when EBV induces a polyclonal B cell activation. Acyclovir treatment is effective in the EBV-genome positive hairy leukoplakia in human immunodeficiency virus-seropositive patients. No effect of antiviral therapy has been reported in the X-linked lymphoproliferative syndrome. Prophylactic use of immunoglobulin or acyclovir has been suggested in susceptible children.
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PMID:Management of Epstein-Barr virus infections. 284 54

The destruction of proliferating lymphoid cells within germinal centers with subsequent replacement by histiocytoid cells has been described in infants and children dying of viral and bacterial infections. The etiology and significance of "epithelioid germinal centers" (EGCs) are unknown. The cells implicated in forming EGCs have included histiocytes and dendritic reticulum cells. We have studied four children at autopsy who died at ages ranging from 10 months to 7 years. Three contracted fatal infections, one with fulminant meningococcemia, one with bacterial sepsis, and one with viral hepatitis. The fourth child contracted viral pneumonitis and died of acetaminophen toxicity. Epithelioid germinal centers were found in numerous lymphoid organs (spleen, lymph nodes, and Peyer's patches) in all four cases. Avidin-biotin complex immunohistochemical analysis performed on formalin-fixed splenic tissue from the first three cases and snap-frozen splenic tissue from the second case revealed an absence of B cells in the follicular centers. The mantle zones surrounding follicles were thin but intact. The histiocytoid cells expanding the germinal centers were positive for S100 and R4/23 (dendritic reticulum cells) and negative for numerous histiocyte markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme). Increased numbers of killer cells (Leu-7) were present within the affected germinal centers in the three cases in which material was available for immunohistochemical studies. Overwhelming infections in these patients seem to result in anomalous natural killer cell activation resulting in localized nonselective destruction of follicular centers similar to anomalous natural killer cell activity reported to occur in fatal infectious mononucleosis. This may lead to an acquired immunodeficiency that precludes long-term survival in affected patients.
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PMID:Epithelioid germinal centers in overwhelming childhood infections. The aftermath of nonspecific destruction of follicular B cells by natural killer cells. 284 41

We have previously shown that antigen-specific T-suppressor (Ts) cells can be generated in vitro by antigens of Epstein-Barr virus (EBV). However, patients with EBV-associated disorders and particularly those with EBV-induced infectious mononucleosis characteristically have nonspecific Ts cells in their peripheral circulation. To explore this apparent paradox, we have now examined the interaction of EBV antigens with either an unrelated antigen (tuberculo-protein-PPD) or a T-cell mitogen (phytohemagglutinin-PHA) in the in vitro generation of Ts cells. Our findings are: (1) the presence of unrelated antigens results in the generation of nonspecific Ts cells in a system wherein an EBV antigen (in excess) alone otherwise induces only antigen-specific Ts cells; (2) the unrelated antigen may be present in a wide range of concentrations and (3) can contribute to nonspecific Ts cell generation when added as long as 2 days after initiation of induction by EBV antigen; (4) the unrelated antigen must be recognized by the sensitized lymphocytes in order for nonspecific Ts cells to be induced; and most interestingly (5) when a second, immunologically different, EBV antigen is substituted for the unrelated antigen (PPD), again nonspecific Ts cells are induced in this system. We propose that the presence of unrelated (or multiple) antigens, in addition to the antigen-specific Ts cell-inducing antigen, contributes to the generation of nonspecific Ts cells in vivo, and that this phenomenon may be important in infections, malignancies, and immunodeficiency states.
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PMID:Epstein-Barr virus immunosuppression: II. Generation of nonspecific suppressor T lymphocytes in vitro. 285 75

The X-linked lymphoproliferative syndrome is triggered by Epstein-Barr virus infection and results in fatal mononucleosis, immunodeficiency, and lymphoproliferative disorders. This study shows that the mutation responsible for X-linked lymphoproliferative syndrome is genetically linked to a restriction fragment length polymorphism detected with the DXS42 probe (from Xq24-q27). The most likely recombination frequency between the loci is 4%, and the associated logarithm of the odds is 5.26. Haplotype analysis using flanking restriction fragment length polymorphism markers indicates that the locus for X-linked lymphoproliferative syndrome is distal to probe DXS42 but proximal to probe DXS99 (from Xq26-q27). It is now possible to predict which members of a family with X-linked lymphoproliferative syndrome are carrier females and to diagnose the syndrome prenatally.
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PMID:Mapping the X-linked lymphoproliferative syndrome. 288 15

We identified 13 patients who contracted acquired immunodeficiency syndrome or human immunodeficiency virus-related disease after a cardiothoracic operation. The operations were performed between January 1981 and November 1984, and the diagnosis of human immunodeficiency virus-related disease was established from 26 to 54 months after operation. The survival time from diagnosis ranged from 8 days to 14 months in the 10 patients who have died. A clinical illness developed in three of the patients immediately postoperatively that was consistent with primary human immunodeficiency virus mononucleosis. The clinical features included a wide variety of opportunistic infections, but an abnormally high percentage of the patients first showed symptoms of dementia or neoplastic disease. In many patients, the diagnosis was not suspected for a prolonged period of time. On the basis of the prolonged incubation period, the incidence of this disease is likely to increase for several more years.
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PMID:Acquired immunodeficiency syndrome, a complication of cardiothoracic surgery. 291 Nov 89

Between August 1985 and June 1987, 809 subjects at risk for AIDS have been studied. 231 (28.5%) were seropositive for human immunodeficiency virus (HIV) antibodies. The seropositivity rate was 41% among drug addicts, 20.5% among homosexual/bisexual males, 19.7% among sexual partners of seropositive individuals. None of 62 subjects belonging to the health care personnel who interacted with seropositive patients and none of the 26 relatives of HIV-infected subject, have been found to be seropositive. Moreover the HIV seropositivity in the population of Parma was only 0.01%. Among the seropositive subjects, 155 (67.1%) were asymptomatic; 2 (0.8%) showed acute infection (a mononucleosis-like syndrome in both, associated with aseptic meningitis in one); 57 (24.6%) had PLG, 7 (3.4%) ARC, 9 (3.8%) full-blown AIDS (8 of these latter are dead).
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PMID:[Acquired immunodeficiency syndrome: epidemiological, clinical and immunological findings in risk groups in Parma]. 297 Jul 56

Antibody titers to Epstein-Barr virus (EBV)-associated early antigens (EA) and the viral capsid antigen (VCA) were determined by ELISA on 263 sera obtained from healthy donors, patients with Hodgkin's disease (HD), non-Hodgkin lymphomas (NHL), infectious mononucleosis (IM), Burkitt's lymphoma (BL), and nasopharyngeal carcinoma (NPC). As expected, most lymphoma patients showed markedly elevated anti-VCA IgG and anti-EA IgG antibody titers. Only one patient in the NHL group (n = 56) consisting of patients with lymphomas other than chronic lymphocytic leukemia (CLL) and hairy-cell leukemia (HCL), and 3 patients with HCL (n = 19) had high antibody titers of the IgA class to VCA and EA. Seventeen out of 48 patients (36%) with CLL had high IgA anti-VCA titers and 10 of these sera (21%) also contained IgA anti-EA. The geometric mean titer (GMT) of IgA anti-VCA was 2,510, the GMT of IgA anti-EA was 780. These antibody titers were about 10 times lower than the corresponding GMT of the NPC patients investigated in this study. The elevated IgG and IgA antibody titers to VCA and EA in CLL and HCL patients seem to reflect an immunodeficiency secondary to the malignant disease leading to reactivation of latent EBV infection. The possibility that at least some of these B-cell lymphomas are associated with EBV cannot be excluded.
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PMID:Increased incidence of IgA antibodies to the Epstein-Barr virus-associated viral capsid antigen and early antigens in patients with chronic lymphocytic leukemia. 301 85


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