ABSTRACT
BACKGROUND: Epstein-Barr virus is a worldwide disease that can cause a wide range of human diseases, the person will become a lifelong carrier of the virus once infected. To investigate the mechanism of Epstein-Barr virus nuclear antigen 2 (EBNA2) on B-lymphocytic activity, sera from 35 patients with infectious mononucleosis and from 34 cases without Epstein-Barr virus infection are collected for experimental analysis. METHODS: Quantitative real-time PCR, western blot, and MTT assays were used to evaluate the relative expression level of EBNA2 and to examine its impact on cell vitality. RESULTS: Research found that the average EBNA2 mRNA and protein levels in 35 patients with infectious mononucleosis were higher than that 34 cases without Epstein-Barr virus infection. The MTT assay indicates that EBNA2 can promote the growth and proliferation of B lymphocytes. CONCLUSIONS: Combining the above implies that EBNA2 plays an important role in diseases that are induced by the Epstein-Barr virus. Other experiments reveal that ATO promotes the degradation of EBNA2 protein and induces the apoptosis of B lymphocytes which are EBNA2-positive.
Subject(s)
B-Lymphocytes/immunology , Epstein-Barr Virus Nuclear Antigens/immunology , Herpesvirus 4, Human/immunology , Infectious Mononucleosis/immunology , Apoptosis/drug effects , Apoptosis/immunology , Arsenic Trioxide/pharmacology , B-Lymphocytes/drug effects , B-Lymphocytes/virology , Cell Proliferation/drug effects , Cell Survival/drug effects , Cell Survival/immunology , Cells, Cultured , Epstein-Barr Virus Nuclear Antigens/genetics , Epstein-Barr Virus Nuclear Antigens/metabolism , Herpesvirus 4, Human/genetics , Herpesvirus 4, Human/physiology , Humans , Infectious Mononucleosis/metabolism , Infectious Mononucleosis/virology , Lymphocyte Activation/drug effects , Lymphocyte Activation/immunology , Viral Proteins/genetics , Viral Proteins/immunology , Viral Proteins/metabolismABSTRACT
Hand, foot, and mouth disease (HFMD) was one of the most common children illnesses. Coxsackievirus A16 was one of the major pathogens that cause HFMD. However, the role of vitamin D underlying this common illness has not been elucidated. Our study examined that vitamin D levels was significantly lower in 33 HFMD patients, compared to 36 healthy children. Unexpectedly, both mRNA and protein expression of VDR were significantly decreased in CA16 infected glioblastoma A172 cells. And overexpression of VDR or vitamin D treatment in CA16 infected glioblastoma A172 cells could reverse the CA16 infection induced cell death, apoptosis or mitochondrial membrane rupture. Therefore, our study, for the first time, demonstrated that vitamin D and VDR could associate with the pathogenesis of HFMD. Thus might provide useful information for HFMD prevention and treatments.