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Chapter 27 : Cytomegalovirus, Varicella-Zoster Virus, and Epstein-Barr Virus

Authors: Sonali K. Sanghavi, David T. Rowe, Charles R. Rinaldo
Content Type: Reference
Publication Year: 2009

Category: Clinical Microbiology; Viruses and Viral Pathogenesis

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Cytomegalovirus, Varicella-Zoster Virus, and Epstein-Barr Virus, Page 1 of 2

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Abstract:

The major immediate-early (IE) promoter (MIEP) of cytomegalovirus (CMV) controls the transcription of IE genes, IE1 and IE2, to encode proteins p72 and p86, respectively. Laboratory-based diagnosis is usually required to identify congenital and perinatal CMV disease and to diagnose and monitor viral levels in immunosuppressed hosts. The laboratory techniques commonly employed are the conventional tube and shell vial viral culture techniques, immunological techniques for histopathology, immunohistochemical techniques, antigen and antibody detection, and nucleic acid detection. Acyclovir, which is successfully used against other herpesviruses, such as herpes simplex virus (HSV) and varicella-zoster virus (VZV), is less potent against CMV. As one's understanding of the CMV genome and protein functions further advances, novel vaccine candidates and strategies will evolve that give equivalent or better humoral and cellular immune responses than natural immunity. The availability and versatility of VZV cosmids, which are large DNA fragments of the viral genome that can be recombined to form replication-competent VZV, have allowed targeting of different ORFs with point deletion mutants. A live attenuated vaccine was most effective in persons 60 to 69 years of age, but it also decreased the severity of incident zoster in people 70 years or older. Epstein-Barr virus (EBV) infection in the immunocompromised host is accompanied by the risk of developing lymphoproliferative disease. Using cytotoxic T lymphocyte (CTL) therapy in combination with other treatment modalities for aggressive PT-LPDs that are unresponsive to reduced immunosuppression has successfully induced remission without significant side effects.

Citation: Sanghavi S, Rowe D, Rinaldo C. 2009. Cytomegalovirus, Varicella-Zoster Virus, and Epstein-Barr Virus, p 454-493. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch27
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Cytomegalovirus, Varicella-Zoster Virus, and Epstein-Barr Virus
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Citation: Sanghavi S, Rowe D, Rinaldo C. 2009. Cytomegalovirus, Varicella-Zoster Virus, and Epstein-Barr Virus, p 454-493. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch27
/content/10.1128/9781555815974.ch27.ch27fig01
FIGURE 1
Antibody responses to EBV antigens during the course of IM are plotted relative to the period of atypical lymphocytosis and virus shedding. Reciprocal titers are shown for the virus-specific IgG class of antibody detected by immunofluorescence assays for the classical EA, VCA, and EBNA.
10.1128/9781555815974/ch27fig7_thmb.gif
10.1128/9781555815974/ch27fig7.gif
Image of FIGURE 1
FIGURE 1

Antibody responses to EBV antigens during the course of IM are plotted relative to the period of atypical lymphocytosis and virus shedding. Reciprocal titers are shown for the virus-specific IgG class of antibody detected by immunofluorescence assays for the classical EA, VCA, and EBNA.

Citation: Sanghavi S, Rowe D, Rinaldo C. 2009. Cytomegalovirus, Varicella-Zoster Virus, and Epstein-Barr Virus, p 454-493. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch27
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