Chapter 25 : Epstein-Barr Virus

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In the century preceding the discovery of Epstein-Barr virus (EBV), physicians speculated that a common clinical syndrome characterized by fever, tonsillar adenopathy, splenomegaly, and mononuclear leukocytosis termed glandular fever was caused by a pathogen (1). In 1920, the name infectious mononucleosis (IM) was introduced by Thomas P. Sprunt and Frank A. Evans to characterize this syndrome (2). Three years later, Hal Downey and C.A. McKinlay described the now-classic atypical lymphocyte as a common feature of this disease (3), and in 1932 John Rodman Paul and Walls Willard Bunnell demonstrated high titers of spontaneously occurring heterophile antibodies in the sera of patients with IM (4), ensuring more accurate diagnosis. In 1961, the British surgeon Denis P. Burkitt gave the first account outside of Africa of “The Commonest Children's Cancer in Tropical Africa” at Middlesex Hospital London, detailing the geographic relationship between Burkitt's lymphoma (BL) and conditions of temperature, altitude, and rainfall associated with development of malaria (5, 6). M. Anthony Epstein, who was in the audience, became intrigued by the idea that a biological agent might be involved in the etiology of BL, and in 1964, the Epstein laboratory analyzed BL biopsy samples by thin-section electron microscopy and discovered a new, large, icosahedral herpesvirus that could be directly reactivated from –grown BL cells (7). These initial findings were reported in and the virus was named after Epstein and his graduate student Yvonne Barr (8). Shortly thereafter, two independent groups (9, 10) demonstrated the ability of EBV to transform primary human B lymphocytes into permanently growing lymphoblastoid cell lines (LCLs), providing the first concrete evidence of the ability of EBV to promote human cancer. In 1968, Gertrude Henle and Werner Henle made two further critical observations: (1) that EBV seroconversion occurred during the course of acute IM (AIM) in a laboratory technician (9) and (2) that EBV-carrying LCLs spontaneously formed from a peripheral blood leukocyte culture obtained during the acute phase of the technician's illness. The Henles confirmed their observations through study of sera provided by James Corson Niederman and Robert W. McCollum, who collected blood from incoming Yale freshmen and later from individuals who developed AIM. This study and others demonstrated EBV-specific antibodies in the sera of the students who developed AIM, confirming the etiologic association between EBV and AIM (11).

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 1

Virion composition and genome organization. (a) Electron micrograph of Epstein-Barr virus (EBV) budding from the plasma membrane (). Diagram of virion components (). (b) Diagram of circular genome (episome) with localization of latent transcripts. (c) Diagram of linear genome displaying localization of BamHI fragments. (Modified from ref. with permission; virion image from Wikipedia.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 2

Following primary infection, Epstein-Barr virus (EBV) in a latent state accompanies its B cell host through the B lymphocyte maturation process, only switching to the lytic cycle and virus production upon plasma cell (terminal) differentiation. (Diagram of B cell differentiation from Quizlet.com and modified by the author to reflect virus biology.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 3

Distinct Epstein-Barr virus (EBV) expression programs (latency III, II, I, 0, lytic replication, abortive replication) are linked with defined stages of B lymphocyte maturation. These same latency patterns are detected in the B cell tumors that arise from transformed cells blocked from further differentiation. Major classes of B cell cancers are indicated in bold. Other EBV-associated tumors that share the indicated latency program but are not of B cell origin are shown in plain font.

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 4

Genomic origin of noncoding RNAs including EBV-encoded RNAs (EBERs), microRNAs (miRNAs), BamHI-A rightward (BART), and an Epstein-Barr virus (EBV) small nucleolar RNA (snoRNA). There is clustering of precursor miRNAs in the BART and to a lesser degree in the BHRF1 region of the genome. (Reproduced from ref. with permission from the journal.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 5

Immunobiology of Epstein-Barr virus (EBV) infection in the normal host. Diagram illustrating the transmission, primary infection, persistent infection, and how the cellular immune response becomes activated to prevent disease. (Reproduced from ref. with permission from the journal.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 6

Classic Epstein-Barr virus (EBV) serologic responses in acute versus remote versus reactivated EBV infection. (Reproduced from ref. with permission from the journal.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 7

Frequency and distribution of CD4 and CD8 T cells in response to lytic and latent cycle Epstein-Barr virus (EBV) proteins. (Reproduced from ref. with permission from the journal.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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Image of FIGURE 8

Acute infectious mononucleosis (AIM). Swollen lymph nodes, pharyngitis, fatigue, and headache comprise the four classic symptoms of AIM (). Pharyngitis is often exudative (), and atypical lymphocytes are present in blood (). (Image of symptoms of AIM https://www.nim.nih.gov//medlineplus/ency/imagepages/17267. Image of atypical lymphocytes from Wikipedia; image of pharyngitis from ref. reproduced with permission from the publisher.)

Citation: Fingeroth J. 2017. Epstein-Barr Virus, p 523-547. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch25
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