Viral Capsid Antigen IgM Antibodies Research Articles

Epstein-Barr Virus: An Infrequent Pathogen of Acute Undifferentiated Febrile Illness From a Tertiary Care Hospital in Southern India.

Context: Acute undifferentiated febrile illness (AUFI) is characterized by a sudden onset of raised body temperature and is a common cause of hospital admission though not recognized as a disease state by the World Health Organization. Epstein-Barr virus (EBV) is reported to account for a significant occurrence of AUFI cases.Aim: To know the role of EBV infection as a cause of acute undifferentiated febrile illness (AUFI).Settings and design: We have used the combination of EBV serological assays to establish the role of the Epstein-Barr virus as the cause of acute undifferentiated febrile illness.Methods and material: A total of 721 suspected cases of acute undifferentiated febrile illness which were tested negative for other common causes of acute febrile illness were selected for the study. Serum samples collected from these cases were tested for the presence of the EBV viral capsid antigen (VCA) IgM antibody. All positive serum samples were tested for the presence of EBV Epstein-Barr nuclear antigen (EBNA) IgG.Statistical analysis used: Statistical analysis was performed with the help of Microsoft Excel software (Microsoft Corporation, Redmond, USA). Results: Out of 721 suspected AUFI cases tested for EBV VCA IgM antibodies, 117 samples were positive and 604 were negative. All these 117 samples were tested for EBV EBNA IgG antibodies in which 88 were positive and 29 were negative. In our study, we found that around 4% (positive for VCA IgM and negative for EBNA IgG) of AUFI cases can be attributed to primary acute EBV infection.Conclusions: EBV infection should be considered particularly in AUFI cases of less than five years of age even in those who do not meet the typical presentation of fever, lymphadenopathy and sore throat. Our study should help to raise awareness regarding the possibility of EBV infection particularly in AUFI cases. A high index of suspicion and timely diagnosis will definitely help clinicians to avoid a battery of investigations and misuse of antibiotics in cases of AUFI.

FcγRIIb Expression Is Decreased on Naive and Marginal Zone-Like B Cells From Females With Multiple Sclerosis.

B cells are critical to the development of multiple sclerosis (MS), but the mechanisms by which they contribute to the disease are poorly defined. We hypothesised that the expression of CD32b (FcγRIIb), a receptor for the Fc region of IgG with inhibitory activities in B cells, is lower on B cell subsets from people with clinically isolated syndrome (CIS) or MS. CD32b expression was highest on post-naive IgM+ B cell subsets in healthy controls. For females with MS or CIS, significantly lower CD32b expression was identified on IgM+ B cell subsets, including naive and IgMhi MZ-like B cells, when compared with control females. Lower CD32b expression on these B cell subsets was associated with detectable anti-Epstein Barr Virus viral capsid antigen IgM antibodies, and higher serum levels of B cell activating factor. To investigate the effects of lower CD32b expression, B cells were polyclonally activated in the presence of IgG immune complexes, with or without a CD32b blocking antibody, and the expression of TNF and IL-10 in B cell subsets was assessed. The reduction of TNF but not IL-10 expression in controls mediated by IgG immune complexes was reversed by CD32b blockade in naive and IgMhi MZ-like B cells only. However, no consequence of lower CD32b expression on these cells from females with CIS or MS was detected. Our findings highlight a potential role for naive and marginal zone-like B cells in the immunopathogenesis of MS in females, which requires further investigation.

Epstein-Barr virus infection with acute acalculous cholecystitis in previously healthy children.

Acute acalculous cholecystitis (AAC), an inflammatory process of the gallbladder (GB) in the absence of gallstones, typically occurs in seriously ill patients. AAC can complicate primary Epstein-Barr virus (EBV) infection, but it is an atypical clinical presentation. The aim of our study was to analyse AAC occurrence in children with primary symptomatic EBV infection who had been admitted to the hospital. We retrospectively evaluated the medical documentation of 181 children with EBV infection who were diagnosed based on the presence of viral capsid antigen IgM antibodies. All EBV-positive patients underwent transabdominal ultrasonography of the liver in the supine and right anterior oblique positions. Fifteen children who presented with AAC symptoms, including abdominal pain and a positive Murphy's sign, were analysed as a subsample and re-evaluated after 2-3months. The incidence of AAC in children hospitalised with infectious mononucleosis (IM) was estimated at 8.3%. Analysis of the laboratory results confirmed that the C-reactive protein (CRP) concentration was the only parameter which was higher in children who presented with AAC symptoms. The mean number of leucocytes and monocytes and liver enzyme activities were not significantly higher. The radiological findings of AAC were evident: increased GB wall thickness, non-shadowing echogenic sludge and pericholecystic fluid collection. AAC during primary EBV infection appears to be a more common pathology than previously suspected. Its relatively mild nature and the lack of laboratory abnormalities mean that ultrasonographic examination is required for diagnosis. This might explain why the prevalence in children is underestimated.

Epstein-Barr Virus Neurologic Complications.

Investigators at the Karol Marcinkowski University of Medical Sciences, Poznan, Poland, analyzed the records of 194 children diagnosed with Epstein-Barr virus infection and having the viral capsid antigen IgM antibody.

Neurologic Complications Caused by Epstein-Barr Virus in Pediatric Patients.

We retrospectively analyzed the medical documentation of 194 children infected with Epstein-Barr virus. The diagnosis was based on clinical symptoms and the presence of the viral capsid antigen IgM antibody. Patients with severe neurologic complications also underwent neurologic examination, magnetic resonance imaging (MRI), and electroencephalography (EEG). There were 2 peaks in incidence of infection; the first one in young children aged 1 to 5 years represented 62.0% of cases. The second peak (24.6% of patients) occurred in teenagers. Febrile seizures were confirmed in 3.1% of affected children younger than 5 years and headaches in 24.2% patients, mostly older children. Ten children presented severe, neurologic complications: meningoencephalitis, acute encephalitis, acute cerebellitis, transverse myelitis, and myeloradiculitis. Our study identified a variety of Epstein-Barr virus-related neurologic complications. Epstein-Barr virus should be routinely tested for when a child presents with an apparent neuroinfection as it is a common pathogen that can induce a wide variety of signs and symptoms.

High-dose dexamethasone therapy for severe thrombocytopenia and neutropenia induced by EBV infectious mononucleosis

Immune thrombocytopenic purpura (ITP) is a hematologic disorder characterized by autoimmune-mediated platelet destruction. Although prednisone (or prednisolone) is generally used for treatment of ITP, high-dose dexamethasone therapy is also effective and leads to rapid recovery of platelet count [1]. In contrast, optimal management of secondary ITP has not been well established. Here, we present a case of significant thrombocytopenia and neutropenia accompanied with Epstein–Barr virus (EBV)induced infectious mononucleosis (IM). A 36-year-old male visited our hospital with 2-week history of sore throat and fever. Physical examination showed cervical lymphadenopathy without hepatosplenomegaly. Peripheral blood findings were as follows: hemoglobin 13.5 g/dL, white blood cell count (WBC) 7.1 9 10/L (22.5% neutrophils, 1.5% monocytes, 6.0% lymphocytes, and 70.0% atypical lymphocytes), platelet count 71 9 10/L, aspartate aminotransferase 177 IU/L, alanine aminotransferase 240 IU/L, and lactate dehydrogenase 564 IU/L. The serological examination for EBV infection revealed the following results: the antibodies for viral capsid antigen (VCA) immunoglobulin (Ig) G was 940, VCA IgM and anti-EB virus nuclear antigen (EBNA) IgG were negative. Also, serum EBV DNA was increased to 4.0 9 10 copies/L. He was diagnosed as EBV-induced IM. His symptom disappeared in a week. However, platelet count continued to decrease, followed by decreased WBC, as shown in Fig. 1. About 60 days after the first symptom appeared, peripheral blood counts were WBC 1.4 9 10/L with 30% neutrophils and platelet count 12 9 10/L. Reticulated platelets were increased to 12.6%. The patient’s serum was positive for anti-neutrophil antibody and platelet-associated IgG (PAIgG) was increased. Antineutrophil antibody was detected by flow cytometry method. Neutrophils from normal donors were incubated with serum from the patient or pooled sera from normal volunteers as a negative control. Then, membrane-bound IgG and IgM antibodies were detected using fluorescein isothiocyanate (FITC)-labeled goat anti-human immunoglobulin. The fluorescence intensity was plotted and judged for positivity. Furthermore, bone marrow was slightly hypercellular, with increased megakaryocytes. Based on these findings, a diagnosis of autoimmune neutropenia and ITP secondary to EBV infection was done. Because thrombocytopenia prolonged and gradually decreased for about 2 months (minimum platelet count of 12 9 10/L), we started treatment with high-dose dexamethasone therapy (40 mg/day for consecutive 4 days orally) and then stopped without tapering. His platelet count increased gradually to 55 9 10/L in 2 weeks after the treatment. Also, neutrophil count improved rapidly and exceeded above 2.0 9 10/L in 3 days. Currently, 4 months after the therapy, he is well with platelet count 100 9 10/L and neutrophil count about 1.0 9 10/L. No adverse effects were noted during and after the therapy. Our patient developed typical symptoms suggestive of IM. Although negative VCA IgM antibody is inconsistent with the present infection, it is reported that VCA IgM antibody by fluorescent antibody test might be negative in 30% of patients with initial EBV infection [2]. In this case, negative EBNA IgG and positive EBV DNA in peripheral blood strongly suggest primary EBV infection. EBV-induced IM is sometimes accompanied by mild Y. Kagoya A. Hangaishi T. Takahashi Y. Imai M. Kurokawa (&) Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan e-mail: kurokawa-tky@umin.ac.jp

<I>Chlamydophila (Chlamydia) pneumoniae</I>との重複初感染が疑われたEpstein-Barr virusによる伝染性単核症の1例

A 26-year-old male was hospitalized with fever and pharyngeal pain. Liver dysfunction and an increase in the percentage of atypical lymphocytes in the peripheral blood were detected. Computed tomography showed pneumonia involving the right lung and synpneumonic pleural effusion. Serum immunological tests showed positive results for Epstein-Barr virus (EBV) viral capsid antigen (VCA) IgM and IgG antibodies and Chlamydophila (Chlamydia) pneumoniae (C. pneumoniae) IgM and IgA antibodies on admission. The pneumonia and pleural effusion were no longer detectable after a week of treatment with starting azithromycin. At 7 weeks after admission, the liver function test results returned to within normal limits, the serum became negative for EBV VCA IgM antibody, the C. pneumoniae IgM antibody titer decreased, and the C. pneumoniae IgA and IgG antibody titers increased. This case was suspected to have infectious mononucleosis caused by primary coinfection with C. pneumoniae and EBV.

高度の黄疸を呈した伝染性単核症の1例

A 28-year-old male was admitted to our hospital with tonsillitis and jaundice. Laboratory findings showed leukocytosis (rate of atypical lymphocytes was 40%), liver dysfunction and hyperbilirubinemia. Epstein-Barr virus (EBV) viral capsid antigen (VCA) IgM and IgG antibodies were positive, and EB nuclear antigen (EBNA) antibody was negative. Abdominal ultrasonography demonstrated hepato-splenomegaly and swelling of intraperitoneal lymph nodes. A diagnosis of infectious mononucleosis was made due to EBV infection. Conservative therapy was given. Total bilirubin and alkaline phosphatase increased to maximum levels of 10.2 mg/dl and 1,590U/l. A liver biopsy specimen revealed infiltration of lymphocytes in sinusoids and portal areas, focal necrosis and intrahepatic cholestasis in parenchyma. Liver function tests returned to normal limits and EBV VCA IgM antibody became negative within 10 weeks from onset.