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Titlebook: Immunobiology and Prophylaxis of Human Herpesvirus Infections; Carlos Lopez,Ryoichi Mori,Richard J. Whitley Book 1990 The Editor(s) (if ap

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Changes in the Epidemiology of Cytomegalovirusparticularly striking during childhood, with rates of seropositivity of 4–6-yr-olds varying from less than 10% in Great Britain and certain populations in the United States to nearly 100% in Africa and the South Pacific. Presumably, these significant differences are the reflection of factors that ac
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Antiviral Activities of a Human Monoclonal Antibody against Human Cytomegalovirus been shown to reduce the incidence of symptomatic CMV infection in transplant recipients (6, 7). Preexisting maternal antibodies also provide some protection against severe CMV infection in newborns (8). These findings suggest that a monoclonal antibody (MAb) of very high titer would provide a pote
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Detection of 12-,-Tetradecanoylphorbol-13-Acetate-induced Cellular Proteins That Compete with the Epzed cell. EBNA-1 has also been implicated in regulation of its own transcription, as well as the transcription regulation of the EBNA family of genes (15, 16). This involvement of EBNA-1 with gene regulation was demonstrated when experiments revealed that the 30-bp repeat region of . functions as a
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Genomic Heterogeneity of Human Herpesvirus 6 Isolatessease of children has not been defined, although preliminary studies have found evidence for changes in HHV-6 serologic status in association with episodes of mild, afebrile illness presenting with symmetrical lymphadenopathy (2). Viral DNA sequences have been found in B-cell lymphoma tissue (3) and
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Replication of Human Herpesvirus 6 (HHV-6): Morphological Aspectsliferative disorders, and subsequently by Lopez et al. (2) and other research groups (3, 4) from individuals seronegative as well as individuals seropositive for human immunodeficiency virus (HIV). Yamanishi et al. (5) probably isolated a different strain of the same virus from the peripheral-blood
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Exanthem Subitum and Human Herpesvirus 6 (HHV-6) Infectionorders (1–5). This virus was initially named “human B lymphotropic virus,” because it infected B lymphocytes (1). However, it was later found mainly to infect and replicate in lymphocytes of T-cell lineage (2, 3, 6, 7). Preliminary characterization of HHV-6 indicated that the virus was antigenically
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