scholarly journals Epstein-Barr Virus (EBV)-associated Haemophagocytic Syndrome

2012 ◽  
Vol 4 (1) ◽  
pp. e2012008 ◽  
Author(s):  
Lorenza Torti ◽  
Luigi Maria Larocca ◽  
Giuseppina Massini ◽  
Luciana Teofili
Keyword(s):  
Epstein Barr Virus ◽  
Multiorgan Failure ◽  
Acute Infection ◽  
Haemophagocytic Syndrome ◽  
Barr Virus ◽  
Ebv Infection ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Epstein Barr

We describe the case of a 17- year old female who developed fatal haemophagocytic syndrome (HPS) one month following acute infection caused by Epstein-Barr virus (EBV). Despite initiation of treatment and reduction of EBV load, laboratory signs of HPS as severe cytopenia, hypofibrinogenemia, hyperferritinemia and hypertriglyceridemia persisted, and the patient died of multiorgan failure. HPS is a rare, but life-threatening complication of EBV infection.

Epstein–Barr virus and regulatory T cells in Egyptian paediatric patients with acute B lymphoblastic leukaemia

2016 ◽  
Vol 70 (2) ◽  
pp. 120-125 ◽  
Author(s):  
Mohamed E Ateyah ◽  
Mona E Hashem ◽  
Mohamed Abdelsalam
Keyword(s):  
Lymphoblastic Leukaemia ◽  
Epstein Barr Virus ◽  
Acute Infection ◽  
Treg Cells ◽  
Control Group ◽  
Healthy Children ◽  
Barr Virus ◽  
Ebv Infection ◽  
High Incidence ◽  
Epstein Barr

ObjectiveAcute B lymphoblastic leukaemia (B-ALL) is the most common type of childhood malignancy worldwide but little is known of its origin. Recently, many studies showed both a high incidence of Epstein–Barr virus (EBV) infection and high levels of CD4+CD25+Foxp3+(Treg cells) in children with B-ALL. In our study, we investigated the possible relationship between EBV infection and the onset of B-ALL, and its relation to expression of CD4+, CD25high+Foxp3+ T regulatory cells.Subject and methodsWe analysed expression and mean fluorescence intensity (MFI) of Treg cells in peripheral blood of 45 children with B-ALL and in 40 apparently healthy children as a control, using flow cytometry. Serum anti-EBV viral capsid antigen (VCA) IgG, anti-EBV nuclear antigen (EBNA) IgG (for latent infection) and anti-EBV VCA IgM (for acute infection) were investigated using ELISA.ResultsAnalysis of the Treg cells population in patients and controls revealed that expression of CD4+ CD25high+ T lymphocytes was higher in patients than in controls (mean±SD 15.7±4.1 and 10.61±2.6 in patients and controls, respectively, and MFI of Foxp3 was 30.1±7.1 and 16.7±3.7 in patients and controls, respectively (p<0.001)). There was a high incidence of latent EBV infection in patients (31%) compared with controls (10%) while the incidence of acute infection was 12% in patients and 0% in the control group. To study the role of latent EBV infection in the pathogenesis of acute B-ALL, OR was calculated (OR=4.06, coefficient index 1.2–13.6).ConclusionsThese findings suggest a possible role for Treg cells and EBV in the pathogenesis of B-ALL. Further studies are needed on the possible mechanisms of tumour genesis related to Treg cells and EBV in children with B-ALL.

scholarly journals Epstein–Barr Virus-Induced Mononucleosis as an Imitator of Severe Preeclampsia

2017 ◽  
Vol 07 (01) ◽  
pp. e5-e7
Author(s):  
S. Staley ◽  
Marcela Smid ◽  
Sarah Dotters-Katz ◽  
Elizabeth Stringer
Keyword(s):  
Differential Diagnosis ◽  
Epstein Barr Virus ◽  
Liver Enzymes ◽  
Acute Infection ◽  
Supportive Treatment ◽  
Barr Virus ◽  
Ebv Infection ◽  
Elevated Liver Enzymes ◽  
Epstein Barr ◽  
In Pregnancy

Background In pregnancy, conditions presenting with hematologic abnormalities, transaminitis, and proteinuria pose diagnostic challenges in pregnancy. Case We present the case of an 18-year-old woman, G1P0, at 33 weeks' gestation with fever of unknown cause, who developed progressively elevated liver enzymes, proteinuria, and thrombocytopenia, due to Epstein–Barr virus (EBV) infection. Conclusion Acute infection with EBV should be included in the differential diagnosis of preeclampsia with severe features, particularly in the setting of fever. Supportive treatment and observation may prevent iatrogenic preterm birth.

scholarly journals Epstein-Barr virus induced sickle hepatopathy

2021 ◽  
Author(s):  
Alison Towerman ◽  
David Wilson ◽  
Monica Hulbert
Keyword(s):  
Organ Failure ◽  
Intrahepatic Cholestasis ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Ebv Infection ◽  
Multi Organ Failure ◽  
First Case ◽  
Life Threatening ◽  
Epstein Barr

Sickle hepatopathy comprises a spectrum of disorders that vary in severity. Intravascular sickling and sinusoidal occlusion are the principal drivers of sickle hepatopathy, but infection or autoimmunity may act as triggers. We describe two cases of acute sickle hepatopathy initiated by primary Epstein-Barr virus (EBV) infection, a previously unreported association. The first case entailed a 14-year-old girl with hemoglobin SC (HbSC) disease who developed hepatic sequestration crisis that responded to a simple transfusion of erythrocytes. The second case was that of a 16-year-old boy with HbSC disease who experienced life-threatening intrahepatic cholestasis with multi-organ failure.

scholarly journals Acute hepatitis: a rare complication of Epstein-Barr virus (EBV) infection

2010 ◽  
Vol 4 (10) ◽  
pp. 668-673 ◽  
Author(s):  
Mehmet Uluğ ◽  
Mustafa Kemal Çelen ◽  
Celal Ayaz ◽  
Mehmet Faruk Geyik ◽  
Salih Hoşoğlu
Keyword(s):  
Liver Function ◽  
Acute Hepatitis ◽  
Epstein Barr Virus ◽  
Acute Infection ◽  
Healthy Woman ◽  
Liver Function Tests ◽  
Barr Virus ◽  
Ebv Infection ◽  
Function Tests ◽  
Epstein Barr

Infectious Mononucleosis (IM), a benign lymphoproliferative disease, is the best known clinical syndrome caused by Epstein-Barr Virus (EBV). It usually resolves over a period of weeks or months without sequelae but may occasionally be complicated by a wide variety of neurologic, hematologic, hepatic, respiratory, and psychological complications. In this report we describe a patient with acute hepatitis following EBV-IM in a previously healthy woman. A 26-year-old woman who presented with fever, generalized weakness, nausea, sore throat, yellowing of skin, and a generalized skin rash was admitted to our clinic. Tonsillar enlargement, pharyngeal erythema, palatal petechiae, lymphadenopathy, and jaundice were noted. Significant atypical lymphocytes ( > 10%) were seen on the peripheral blood smear. Liver function tests such as ALT: 303 U/L, AST: 172 U/L, ALP: 193 U/L and total bilirubin: 7.3 mg/dl were elevated. Serological tests for EBV infection were consistent with acute infection (EBV virus capsid antigen was reactive with IgM and IgG antibodies). The Monospot test was also positive. On the seventh day, liver function tests and bilirubin had risen to peak level and platelets were decreased. The patient was managed supportively and her critical condition improved and was finally stabilized. Although the prognosis for IM is very favorable, a variety of acute complications may occur.

scholarly journals P-O12 Atraumatic Splenic Rupture Secondary to Concurrent Cytomegalovirus and Epstein Barr Virus Infection

2021 ◽  
Vol 108 (Supplement_9) ◽  
Author(s):  
Catherine McCollum ◽  
Khurram Khan ◽  
Dhruv Sahni ◽  
David Bell ◽  
David Chong
Keyword(s):  
Epstein Barr Virus ◽  
Splenic Rupture ◽  
Sudden Onset ◽  
Cmv Infection ◽  
Barr Virus ◽  
Ebv Infection ◽  
Life Threatening ◽  
History Of ◽  
Epstein Barr ◽  
Atraumatic Splenic Rupture

Abstract Background Infectious Mononucleosis (IM) is a common viral illness among adolescents and young adults. While most cases are self-limiting, a small number of patient can develop life threatening complications, such as atraumatic splenic rupture (ASR). This is a rare but serious sequelae, and the commonest cause of associated mortality. While Epstein Barr Virus is commonly associated with IM, concurrent infection of cytomegalovirus (CMV) and EBV is rarely reported.  Both infections are associated with splenomegaly, however this is usually mild and very rarely results in ASR. Methods We present the case of an immunocompetent nineteen year old male who underwent emergency splenectomy for ASR secondary to concurrent EBV and CMV infection. He presented to the Emergency Department with a five hour history of severe, sudden onset left upper quadrant pain preceded by coughing fit. He reported a one year history of incidental splenomegaly and recent positive monospot test in community. Computerised tomography (CT) of abdomen and pelvis confirmed splenic rupture with large haemo-peritoneum and large sub-capsular haematoma. He was haemodynamically unstable and underwent laparotomy and splenectomy. Results Intraoperative findings included two litres of intraperitoneal blood and large spleen with sub-capsular haematoma; approximately seventeen centimetre diameter and weighed nine hundred and seventy grams. Pathology showed features of non-specific lymphoid hyperplasia. Serum virology confirmed high levels of CMV on polymerase chain reaction with low levels of EBV detected. Virology screening was incidentally repeated post discharge and at this time was consistent acute EBV infection. No alternative cause for splenic rupture or pre-existing splenomegaly has been identified. Conclusions The serology results in this case confirm acute CMV infection with most likely concurrent EBV infection. While we cannot confidently identify which virus caused splenic rupture in this case, ASR is a life threatening condition and an important differential in patients presenting with sudden onset LUQ pain and shock. Splenectomy remains the treatment of choice in haemodynamically unstable patients.

scholarly journals Autoimmune hepatitis following Epstein-Barr virus infection: a diagnostic dilemma

2019 ◽  
Vol 12 (7) ◽  
pp. e229615 ◽  
Author(s):  
Haoran Peng ◽  
Tanna Lim ◽  
Jae Nam ◽  
Jin Lee
Keyword(s):  
Autoimmune Hepatitis ◽  
Epstein Barr Virus ◽  
Case Reports ◽  
Acute Infection ◽  
Epstein Barr Virus Infection ◽  
Diagnostic Dilemma ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr ◽  
Barr Virus Infection

Epstein-Barr virus (EBV) infections frequently affect the liver and cause hepatitis. EBV is a well-known trigger of certain autoimmune diseases. There are few case reports showing the evidence of autoimmune hepatitis (AIH) following EBV infection. However, the diagnosis of AIH is very challenging in the setting of an acute infection. Here, we demonstrate a case of AIH following EBV infection in a patient ultimately recovered after receiving treatment for AIH.

Epstein–Barr virus infection in primary immunodeficiency

2018 ◽  
Vol 5 (3) ◽  
pp. 65-85 ◽  
Author(s):  
Adi Ovadia ◽  
Ilan Dalal
Keyword(s):  
Primary Immunodeficiency ◽  
Epstein Barr Virus ◽  
Current Knowledge ◽  
Acute Infection ◽  
Epstein Barr Virus Infection ◽  
Barr Virus ◽  
Ebv Infection ◽  
Increased Risk ◽  
Abnormal Response ◽  
Epstein Barr

Primary immunodeficiency (PID) is a group of genetic disorders which affects immune cell development, differentiation, and function. The affected individuals are highly susceptible to infection by a diverse array of pathogens. Epstein–Barr virus (EBV) infection is ubiquitous in humans and usually involves an asymptomatic or self-limiting clinical course. In rare cases, EBV can cause not only an acute infection but also a severe exaggerated immune response and lymphoproliferative disease. Furthermore, EBV infection in patients with PID can lead to immune dysregulation and increased risk of malignancies, in addition to the severe course of the acute infection. Recognition of the different genetic defects and their effect on immunological pathways provide us with fundamental insights into the pathophysiology of EBV infection and associated disease, and may lead to developing better targeted therapies in the future. Here, we review all of PIDs with an abnormal response to EBV disease. Statement of novelty: Here we provide a review of the current knowledge of all PIDs reported to be associated with abnormal response to EBV infection and associated disease, such as hemophagocytic lymphohistiocytosis.

Glandular fever and Epstein-Barr virus-related polyneuropathy: a life-threatening complication

2020 ◽  
Vol 13 (10) ◽  
pp. e235678
Author(s):  
Colm Brendan Dorris ◽  
Donna Gallagher ◽  
Myles Black
Keyword(s):  
Epstein Barr Virus ◽  
Upper Airway ◽  
Surgical Tracheostomy ◽  
Barr Virus ◽  
Glandular Fever ◽  
Life Threatening ◽  
History Of ◽  
Life Threatening Complication ◽  
Epstein Barr ◽  
Multiple Cranial Nerve

An 18-year-old woman presented with a 1-week history of sore throat, lethargy and fevers. She was subsequently diagnosed with glandular fever and was managed conservatively. Following 1 week of conservative measures, she developed acute upper airway obstruction requiring emergency surgical tracheostomy insertion. Further investigation including electromyography demonstrated multiple cranial nerve neuropathies.

scholarly journals Mouse model for acute Epstein–Barr virus infection

2016 ◽  
Vol 113 (48) ◽  
pp. 13821-13826 ◽  
Author(s):  
Tristan Wirtz ◽  
Timm Weber ◽  
Sven Kracker ◽  
Thomas Sommermann ◽  
Klaus Rajewsky ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Expansion ◽  
Epstein Barr Virus ◽  
T Cell Response ◽  
Barr Virus ◽  
Ebv Infection ◽  
Life Threatening ◽  
Epstein Barr

Epstein–Barr Virus (EBV) infects human B cells and drives them into continuous proliferation. Two key viral factors in this process are the latent membrane proteins LMP1 and LMP2A, which mimic constitutively activated CD40 receptor and B-cell receptor signaling, respectively. EBV-infected B cells elicit a powerful T-cell response that clears the infected B cells and leads to life-long immunity. Insufficient immune surveillance of EBV-infected B cells causes life-threatening lymphoproliferative disorders, including mostly germinal center (GC)-derived B-cell lymphomas. We have modeled acute EBV infection of naive and GC B cells in mice through timed expression of LMP1 and LMP2A. Although lethal when induced in all B cells, induction of LMP1 and LMP2A in just a small fraction of naive B cells initiated a phase of rapid B-cell expansion followed by a proliferative T-cell response, clearing the LMP-expressing B cells. Interfering with T-cell activity prevented clearance of LMP-expressing B cells. This was also true for perforin deficiency, which in the human causes a life-threatening EBV-related immunoproliferative syndrome. LMP expression in GC B cells impeded the GC reaction but, upon loss of T-cell surveillance, led to fatal B-cell expansion. Thus, timed expression of LMP1 together with LMP2A in subsets of mouse B cells allows one to study major clinically relevant features of human EBV infection in vivo, opening the way to new therapeutic approaches.

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