| Research Abstract |
Severe chronic active Epstein-Barr virus (EBV) infection syndrome (SCAEBV) is characterized by persistent or recurrent fever, lymph adenopathy, and hepatosplenomegaly. Laboratory data shows the tendency of pancytopenia and polyclonal gammopathy. Antibody titers against EBV replicating antigens such as viral capsid antigen (VCA) and early antigens (EA) are generally shown to be extremely high, and affected tissues are positive for EBV genome. Furthermore, patients with SCAEBV have very poor prognosis particularly owing to the development of EBV-positive T cell malignancies. A head investigator studied whether EBV and adenovirus type II (ADVII) coinfections occur in these patients by in vitro experiment because both EBV and ADVII were often identified from their tissue materials.
Five patients with SCAEBV were studied. All patients had antibodies against ADVII. Two cases showed increased numbers of both CD8-DR positive cells, two both CD4-DR positive cells, one both CD20-CD23 positive cel
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ls in their circulation, respectively. All these activated cells were positive for EBV genome. Two of them were positive for ADVII genome, as well. Following exogenous infection by either EBV or ADVII, no increased genome positive T cells were significantly demonstrated. No continuous lymphoblastoid cell lines were established either spontaneously from the patients because cytopathic effects (CPE) occurred remarkably. Notably, low interferongamma production was observed in all cultures.
These results suggested activated EBV infection underlain associated with defect of immunosurveillance in patients with SCAEBV. Although no absolute conclusion was evidenced, CPE shown in cultures highly indicated the presence of some lymphotropic viruses including ADVII. Additionally, some heterogeneity was observed in subpopulation regarding the activated EBV infected cells, which may contribute to the development of disease. The degree of severity and the time of disease process are possibly important to clarify the pathogenetic mechanisms in patients with SCAEBV. Less
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