EPSTEIN-BARR VIRUS AND HUMAN HERPESVIRUS TYPE 6 NLM AIDSLINE Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.

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EPSTEIN-BARR VIRUS AND HUMAN HERPESVIRUS TYPE 6

Antiviral Agents and Viral Diseases in Man. Third Edition. Galasso GJ et al, eds. New York, Raven, p. 647-68, 1990.. Unique Identifier : AIDSLINE ICDB/91676217
Straus SE; Medical Virology Section, Lab. of Clinical Investigation, Natl.; Inst. of Allergy and Infectious Diseases, Bethesda, MD 20892

Abstract: All human herpesviruses infect and replicate within lymphocytes to some extent, but Epstein-Barr virus (EBV) and human herpesvirus type 6 (HHV-6) do so efficiently. The pathogenesis and host responses to infection with EBV (and perhaps with HHV-6) depend more on lymphocytic infection than is evident with other human herpesviruses. EBV and HHV-6 are reviewed including history, description of the agent, epidemiology, diagnosis, clinical manifestations, and treatment. The paradigmatic EBV-induced illness is acute infectious mononucleosis (AIM). EBV is associated with malignancies, disorders in immunodeficient patients, chronic mononucleosis, and chronic fatigue syndrome. EBV replication is inhibited effectively in vitro by some nucleoside analogs, including acyclovir (ACV) and ganciclovir (DHPG), and the interferons. Controlled studies in AIM have been undertaken only with ACV. In AIM, ACV markedly reduces the rates of salivary shedding of virus. The effect is transient, however; once treatment is completed, high rates of shedding resume. Little or no symptomatic improvement can be attributed to ACV. The one EBV-associated disorder in which a role for antiviral therapy seems proven is oral hairy leukoplakia. Iv and oral ACV and an oral acyclovir prodrug (6-deoxyacyclovir) each induce marked remissions in hairy leukoplakia lesions, but the lesion often recurs after completion of therapy. A vaccine against EBV appears feasible and populations at risk for EBV-associated malignancies should be the first targets of controlled vaccine trials. No clinical diseases are known to be caused by HHV-6, but four syndromes are associated with the virus: (1) reactivation of HHV-6 in the setting of AIDS, (2) lymphoproliferative disorders, (3) roseola infantum (Exanthem subitum), and (4) chronic fatigue syndrome. There are no specific treatments for HHV-6-associated infections. Fortunately, most infections probably warrant nothing more than symptomatic care. Preliminary studies indicate HHV-6 to be resistant in vitro to clinically attainable concentrations of ACV and DHPG. Since both of these agents are activated by deoxypyrimidine (thymidine) kinases, their failure to inhibit HHV-6 replication suggests that this virus lacks the enzyme and fails to induce further expression of the cellular kinase. HHV-6 replication in cultured lymphocytes is impaired, however, by DNA polymerase inhibitors that do not require enzymatic activation. Preliminary studies have shown complete prevention of HHV-6 late protein synthesis in HSB-2 cells treated with 20 ug/ml foscarnet. (135 Refs)
Keywords: Acquired Immunodeficiency Syndrome/DRUG THERAPY Antiviral Agents/*THERAPEUTIC USE Herpesviridae Infections/*DRUG THERAPY Herpesvirus 4, Human/*DRUG EFFECTS Herpesvirus 6, Human/*DRUG EFFECTS Human Opportunistic Infections/DRUG THERAPY Tumor Virus Infections/DRUG THERAPY Virus Activation/DRUG EFFECTS Virus Replication/DRUG EFFECTS MONOGRAPH REVIEWKWDacquiredimmunodeficiencysyndrome/drugtherapyantiviralagents/KWDtherapeuticuseherpesviridaeinfections/KWDdrugtherapyherpesvirus4,human/KWDdrugeffectsherpesvirus6,human/KWDdrugeffectshumanopportunisticinfections/drugtherapytumorvirusinfections/drugtherapyvirusactivation/drugeffectsvirusreplication/drugeffectsmonographreview
912130
M91C4105

Copyright © 1991 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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