Chronic Infectious Mononucleosis

Isaacs, Raphael

doi:10.1182/blood.v3.8.858.858

Cited by 89 publications

(19 citation statements)

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“…Epstein-Barr virus is also sometimes associated with CAEBV. [1][2][3] Patients with CAEBV occasionally develop a fulminant course with lymphoid malignancy and/or hemophagocytic syndrome. 6 In the present study, five of six cases with CAEBV died due to either hemophagocytosis or lymphoid malignancy.…”

Section: Discussionmentioning

confidence: 99%

CD95 (Fas) ligand expression of Epstein‐Barr virus (EBV)‐infected lymphocytes: A possible mechanism of immune evasion in chronic active EBV infection

Ohshima

Suzumiya

Sugihara

et al. 1999

Pathology International

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The Epstein-Barr virus (EBV) induces infectious mononucleosis (IM) and can be associated with chronic active EBV infection (CAEBV). Cytotoxic T lymphocytes (CTL) play an important role in excluding EBV-infected cells. Two cytotoxic mechanisms of CTL have been demonstrated: one perforin/granzyme-based and the other Fas (CD95)/Fas ligand (FasL)-based. To clarify these two pathways in CAEBV, we analyzed six patients with CAEBV and four patients with IM using immunohistochemical staining of the lymph nodes. In both CAEBV and IM, CD8+ T-cells increased in number, but CD56+ natural killer cells were rare. In four of six cases with CAEBV, approximately half the lymphocytes were positive for T cell-restricted intracellular antigens (TIA-1), which were recognized by the cytolytic granules of CTL. In IM, the number of TIA-1 positive cells was smaller than that in CAEBV. Fas-positive lymphocytes were frequently encountered in both CAEBV and IM. However, FasL-positive lymphocytes increased in three of six patients with CAEBV, but not in patients with IM. Except for one case with CAEBV, the number of perforin- and/or granzyme-positive cells was small in number in both CAEBV and IM cases. In double-staining FasL and EBV in situ hybridization, FasL-positive EBV-infected lymphocytes were detected in CAEBV but not in IM. In CAEBV, the Fas/FasL pathway and not perforin pathways appears to play an important role in the pathogenesis. The data suggest that EBV-infected lymphocytes may evade immune attack through the expression of FasL.

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Section: Discussionmentioning

confidence: 99%

CD95 (Fas) ligand expression of Epstein‐Barr virus (EBV)‐infected lymphocytes: A possible mechanism of immune evasion in chronic active EBV infection

Ohshima

Suzumiya

Sugihara

et al. 1999

Pathology International

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“…CAEBV was originally reported as a condition marked by sustained inflammatory symptoms such as fever, lymphadenopathy and liver dysfunction (the so-called infectious mononucleosis [IM]-like symptoms) associated with high titers of anti-EBV antibodies in the peripheral blood (PB). The first report pertaining to suspected CAEBV was a case-series report of 53 patients in the US in 1948 [2]. The patients who had fever and splenomegaly lasting 'from three months to longer than four years after the initial attack' were diagnosed as having chronic IM.…”

Section: History Of Caebvmentioning

confidence: 99%

Chronic active Epstein–Barr virus infection: a bi-faceted disease with inflammatory and neoplastic elements

Arai

2018

Immunological Medicine

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Chronic active Epstein-Barr virus infection (CAEBV) is one of the Epstein-Barr virus (EBV)positive T-or NK-cell lymphoproliferative diseases. It is characterized by clonal proliferation of EBV-infected T or NK cells and their infiltration into systemic organs, leading to their failure. Inflammatory symptoms, fever, lymphadenopathy and liver dysfunction are main clinical findings of CAEBV. EBV itself contributes to the survival of the host cells via induction of CD40 and CD137 expression and constitutive activation of NF-jB. Accumulation of gene mutations in the infected cells may lead to the development of highly malignant lymphoma or leukemia. Furthermore, constitutive activation of STAT3 is detected in the infected cells, which not only promotes cell survival but also enhances production of inflammatory cytokines. Currently, allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only effective treatment strategy for eradication of EBV-infected T or NK cells. However, active disease at the time of allo-HSCT (defined as presence of fever, liver dysfunction, progressive skin lesions, vasculitis or uveitis) is a negative prognostic factor. Establishment of chemotherapy regimens for effective resolution of disease activity in patients with CAEBV is a key imperative. Based on the recently unraveled molecular mechanisms CAEBV development, pathways mediated by NF-jB or JAK/STAT are potential novel therapeutic targets.

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“…In the laboratory setting, intranasal infection with a luciferase expressing MHV68 indicated viral replication and presence in the cervical draining lymph nodes, the lungs, the spleen (splenomegaly) and vagina during female C57BL/6 infections . Splenomegaly is observed in EBV‐infected patients experiencing IM , and viral titres have also been detected in female and male genital secretions . Intranasal infection of C57BL/6 mice consists of an acute lytic replication in the lungs, peaking around 4–6 days and cleared by day 12 post‐infection.…”

Section: Can Gammaherpesviruses Alter the Pathogenesis Of Malarial Inmentioning

confidence: 99%

Does EBV alter the pathogenesis of malaria?

Matar

Jacobs

Speck

et al. 2015

Parasite Immunology

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Plasmodium falciparum infections have been implicated in immune deficiencies resulting in ineffective control of Epstein-Barr virus, thereby increasing the risk of endemic Burkitt lymphoma in children. However, the impact of Epstein-Barr virus infections on the development of immunity to P. falciparum has not been studied in depth. In this review, we examine novel findings from animal co-infection models and human immuno-epidemiologic studies to speculate on the impact of acute gammaherpesvirus co-infection on malarial disease severity. Children are often concurrently or sequentially infected with multiple pathogens, and this has implications for understanding the development of protective immunity as well as in the evaluation of vaccine efficacy.

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Chronic Infectious Mononucleosis

Cited by 89 publications

References 0 publications

CD95 (Fas) ligand expression of Epstein‐Barr virus (EBV)‐infected lymphocytes: A possible mechanism of immune evasion in chronic active EBV infection

CD95 (Fas) ligand expression of Epstein‐Barr virus (EBV)‐infected lymphocytes: A possible mechanism of immune evasion in chronic active EBV infection

Chronic active Epstein–Barr virus infection: a bi-faceted disease with inflammatory and neoplastic elements

Does EBV alter the pathogenesis of malaria?

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