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Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
Published on: November 8, 2011
Antiviral treatment of Epstein-Barr virus-associated lymphoproliferations
Stephan H Oertel1, Hanno Riess
1Hämatologie und Onkologie, Humboldt-Universität Berlin, Charité Campus Virchow-Klinikum, Germany.
Epstein-Barr virus (EBV)-associated lymphoproliferations may arise in individuals with hereditary or acquired immunodeficiencies. T-cell dysfunction and resulting insufficient control of EBV infection is common to all these patients in whom EBV-associated lymphoproliferations develop. EBV is an oncogenic virus which induces proliferation and transformation of B-lymphocytes. Antiviral treatment may represent a causal treatment option with relatively low toxicity. Among the different antiviral drugs aciclovir and ganciclovir are not the drugs of choice, because in EBV-associated lymphoproliferations the viral thymidine kinase enzyme is not encoded regularly. The agent arginine butyrate has the ability to selectively activate EBV thymidine kinase genes in EBV-infected lymphoma cells. In combination with ganciclovir it has demonstrated efficacy in patients with EBV-associated lymphoproliferations after solid organ transplantation. The action of foscarnet, another antiviral agent, is directed against the viral DNA, independent of the presence of the viral thymidine kinase. In our experience treatment with foscarnet resulted in continuous complete remissions in patients with EBV-associated lymphoproliferations. These clinical experiences demonstrate the efficacy of antiviral treatment in EBV-associated lymphoproliferations.
Epstein-Barr virus (EBV)-associated lymphoproliferations may arise in individuals with hereditary or acquired immunodeficiencies. T-cell dysfunction and resulting insufficient control of EBV infection is common to all these patients in whom EBV-associated lymphoproliferations develop. EBV is an oncogenic virus which induces proliferation and transformation of B-lymphocytes. Antiviral treatment may represent a causal treatment option with relatively low toxicity. Among the different antiviral drugs aciclovir and ganciclovir are not the drugs of choice, because in EBV-associated lymphoproliferations the viral thymidine kinase enzyme is not encoded regularly. The agent arginine butyrate has the ability to selectively activate EBV thymidine kinase genes in EBV-infected lymphoma cells. In combination with ganciclovir it has demonstrated efficacy in patients with EBV-associated lymphoproliferations after solid organ transplantation. The action of foscarnet, another antiviral agent, is directed against the viral DNA, independent of the presence of the viral thymidine kinase. In our experience treatment with foscarnet resulted in continuous complete remissions in patients with EBV-associated lymphoproliferations. These clinical experiences demonstrate the efficacy of antiviral treatment in EBV-associated lymphoproliferations.
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