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      Induction of interleukin-10 on activation of Epstein-Barr virus in EBV-infected B-cell lines.

      Viral immunology
      Acyclovir, pharmacology, Antiviral Agents, B-Lymphocytes, drug effects, virology, Cell Line, Gene Expression, Herpesvirus 4, Human, growth & development, Humans, Immunoglobulin G, immunology, Interleukin-10, biosynthesis, genetics, Phosphonoacetic Acid, Protein-Tyrosine Kinases, antagonists & inhibitors, RNA, Messenger, Virus Activation

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          Abstract

          Human (h) interleukin-10 (IL-10) exhibits a strong DNA and amino acid sequence homology to the Epstein-Barr virus (EBV) BCRF1 genome, viral (v) IL-10. We analyzed the production of IL-10 for EBV activation in B-cell lines. The latent EBV in Akata cells was activated by the cross-linking of surface immunoglobulin G (IgG) with anti-human IgG. The levels of IL-10(h+v) and vIL-10 in the culture fluids were measured by a specific enzyme-linked immunosorbent assay (ELISA). IL-10(h+v) was detected at the same time for EBV immediate early gene BZLF1 product ZEBRA and early gene BMRF1 product EA-D. This was more than 4 hours prior to the appearance of vIL-10, and late gene products gp 350/220 and viral capsid antigen. The induction of hIL-10 and vIL-10 mRNAs were detected in anti-IgG-treated Akata cells by reverse transcription-polymerase chain reaction. The induction of IL-10(h+v) and vIL-10 was inhibited with a tyrosine kinase inhibitor, herbimycin, or with an inhibitor of herpesvirus DNA polymerase, phosphonoacetic acid, or acyclovir. IL-10(h+v) and vIL-10 were also detected in the supernatants of Akata and Daudi but not Ramos cells infected with P3HR-1 EBV. These results show the IL-10 induction on EBV activation in EBV-carrying B-cell lines.

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