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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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Differentiation between the Oka Varicella Vaccine Virus and American Wild-Type Varicella-Zoster Virugnated the Oka strain after the child from whom the virus was isolated. Attenuation was believed to have been induced by serial passage of the original clinical isolate at various temperatures and in different cell lines (1, 2). Numerous studies throughout the world have subsequently shown the vacci
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The T-Lymphocyte Response to Varicella-Zoster Viral Proteinsildren with congenital or acquired T-cell deficiencies (1). The frequent occurrence of herpes zoster with suppression of cellular immunity implies that such immunity is also required to prevent symptoms due to viral reactivation. When a VZV antigen preparation made from sonicated infected cells was
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A Possible Role for Glycoprotein gpV in the Pathogenesis of Varicella-Zoster Virusy infection and shingles (zoster) upon reactivation from the latent state. A number of considerations make it clear that our knowledge of the natural history of this virus must be expanded. First, the increasing age of the general population in the United States is likely to lead to an increase in c
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Changes in the Epidemiology of Cytomegalovirus infection in every population that has been tested, including remote Indian tribes in the Amazon basin that lacked evidence of past measles or influenza infections (2, 3). CMV infection is endemic and without seasonal variation. Climate does not affect the prevalence of infection, and there are no
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Antiviral Activities of a Human Monoclonal Antibody against Human Cytomegaloviruspromised hosts such as recipients of organ or bone marrow transplants (1, 2), patients with acquired immunodeficiency syndrome (3), and newborn babies (4). The immune mechanisms which restrict human CMV infections are thought to involve cellular immune response more than humoral immune response. Thi
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Topological Effects of EBNA 1 on ,, and there must be mechanisms to inhibit the expression of those replicative functions which would ordinarily lead to cell death. In the specific case of the Epstein-Barr herpesvirus (EBV), the genome is maintained by an interaction between EBNA 1 and a region of EBV DNA called . (1–3). This intera
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Epstein-Barr Virus, Burkitt’s Lymphoma, and an African Tumor Promoterth certain B-cell malignancies in man, such as Burkitt’s lymphoma (BL) in tropical Africa and opportunistic lymphomas in immunodeficiency (1–3). The vast majority of the African BL cases are positive for EBV genomic DNA and also for specific reciprocal chromosome translocations mostly between chromo
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Regulation of Expression of the Glycoprotein Genes of Herpes Simplex Virus Type 1 (HSV-1)egulated and sequentially ordered cascade manner (1, 2). The a genes are transcribed by the RNA polymerase II of the host cell in the absence of newly synthesized viral proteins. Functional a proteins are necessary for the transcription of . and . genes (1, 2). The Q products are involved in the rep
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