Strategies Involved in Developing an Effective Vaccine for EBV-Associated Diseases

作者: Denis J. Moss , Christopher Schmidt , Suzanne Elliott , Andreas Suhrbier , Scott Burrows

DOI: 10.1016/S0065-230X(08)60864-7

关键词: GeneGenomeVirusAntigenLymphoproliferative disordersVirologyMononucleosisImmunofluorescenceLatency (engineering)BiologyImmunology

摘要: Publisher Summary This chapter first considers EBV host–virus relationships and then proceeds to discuss the immune control of infection. Epstein–Barr virus (EBV) is encoded by a linear, double-stranded DNA genome 172 kb that includes almost 100 identified open reading frames. The maintains lifelong latent association with B lymphocytes permissive stratified epithelium in oropharynx. Two major subtypes have been identified, A type (also known as EBV-1 EBV-2). It possible characterize three distinct forms latency (latency I, II, III) are distinguished on basis expression genes promoter usage. These patterns or programs form convenient means classifying EBV-associated diseases for vaccine development. humoral response infection defined terms set immunofluorescence assays quantitatively assessed antibody capsid antigen (VCA), membrane (MA), early antigen-restricted (EA-R), antigen-diffuse (EA-D), EBV-induced nuclear antigens (EBNA). Significantly increased shedding oropharynx immunosuppressed individuals provides evidence support an important role T cells controlling unlikely single applicable all will be developed near future. Given variety potential targets III problems recognition II I diseases, vaccines against infectious mononucleosis (IM) posttransplantation lymphoproliferative disorders (PTLD) would seem offer best opportunity Vaccine trials other may need proceed more caution dependent emergence novel strategies derived from either animal models related viruses.

参考文章(197)
M. Rowe, D. T. Rowe, C. D. Gregory, L. S. Young, P. J. Farrell, H. Rupani, A. B. Rickinson, Differences in B cell growth phenotype reflect novel patterns of Epstein-Barr virus latent gene expression in Burkitt's lymphoma cells. The EMBO Journal. ,vol. 6, pp. 2743- 2751 ,(1987) , 10.1002/J.1460-2075.1987.TB02568.X
J.H.C. Ho, Nasopharyngeal Carcinoma (NPC) Advances in Cancer Research. ,vol. 15, pp. 57- 92 ,(1972) , 10.1016/S0065-230X(08)60372-3
D Liebowitz, Nasopharyngeal carcinoma: the Epstein-Barr virus association Seminars in Oncology. ,vol. 21, pp. 376- 381 ,(1994)
Kwok-Wai Lo, D. P. Huang, Sai-Wah Tsao, Chi-Ho Mok, J. C. K. Lee, P. H. K. Choi, Yu-Xi Liu, p53 mutation in human nasopharyngeal carcinomas. Anticancer Research. ,vol. 12, pp. 1957- 1963 ,(1992)
Gertrude Henle, Evelyne T. Lennette, Margaret A. Alspaugh, W. Henle, Rheumatoid factor as a cause of positive reactions in tests for Epstein–Barr virus-specific IgM antibodies Clinical and Experimental Immunology. ,vol. 36, pp. 415- 422 ,(1979)
P. J. Coates, G. Slavin, Gufaraz Khan, R. K. Gupta, Epstein-Barr virus infection and bcl-2 proto-oncogene expression. Separate events in the pathogenesis of Hodgkin's disease? American Journal of Pathology. ,vol. 143, pp. 1270- 1274 ,(1993)
D. V. Ablashi, P. H. Levine, G. R. Pearson, S. D. Kottaridis, Epstein-Barr Virus and Associated Diseases ,(2011)