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Chapter 23 : Cytomegalovirus

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Cytomegalovirus, Page 1 of 2

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Abstract:

Human cytomegalovirus (HCMV) was first isolated in the mid-1950s, when the new technology of cell culture became available. It was isolated independently by three different investigators and named because of its cytopathic effect (CPE), which produced large, swollen, refractile cells causing “cytomegaly.” The virus is ubiquitous, having infected most individuals by early adulthood in developing countries and by late adulthood in developed countries. Most individuals show no symptoms as a result of primary infection, reactivation, or reinfection, indicating that the virus is well adapted to its normal host, which commits substantial immune resources to controlling HCMV. However, in individuals whose immune system is either immature (as in the fetus) or compromised by immunosuppressive therapy or human immunodeficiency virus (HIV) infection, HCMV can cause serious end-organ disease (EOD). Furthermore, accumulation of HCMV-specific T cells over decades contributes to immunosenescence. Thus, HCMV acts as an opportunist, damaging the very young and the very old as well as adults and children whose immune systems are impaired.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Figures

Image of FIGURE 1
FIGURE 1

Schematic representation of glycoprotein B from HCMV. A: The locations of the known antigenic domains (AD) mapped onto gB. B: Linear representation of domain architecture. C: gB monomer, trimer, and three-dimensional representation showing domains. AD1 is a linear, immunodominant epitope, AD2 a linear epitope, AD3 a linear epitope located where the transmembrane portion of gB abuts the cytoplasmic portion, AD4 a discontinuous epitope, and AD5 a discontinuous epitope. SP, signal peptide; TM, transmembrane domain; CD, cytoplasmic domain; dom, domain. Adapted from Potzch (2011) vol 7, issue 8; e1002172.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 2
FIGURE 2

Consensus genetic map of wild-type HCMV based on the Merlin genome. RL and RS (which contain the sequence as a direct repeat at the genome termini and as an inverted repeat internally) are shown in a thicker format than UL and US. Protein coding regions are indicated by colored arrows grouped according to the key, with gene nomenclature shown below. Introns are shown as narrow white bars. Genes corresponding to those in AD169 RL and RS are given their full nomenclature, but the UL and US prefixes have been omitted from UL1–UL150 (12 to 194 kbp) and US1–US34A (199 to 231 kbp). Colors differentiate between genes on the basis of conservation across the , , and (core genes) or between the and (sub core genes), with subsets of the remaining noncore genes grouped into gene families. GPCR, G protein coupled receptor. (Reprinted from reference with permission).

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 3
FIGURE 3

The major IE region of HCMV showing the splicing events that produce distinct proteins. TA, transcriptional activation; PA, polyadenylation; l.mRNA, late mRNA.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 4
FIGURE 4

Regulation of the major IE region of HCMV. CRS, repression sequence.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 5
FIGURE 5

Effect of HCMV proteins on display of mature HLA complexes at the plasma membrane (PM). TAP, transporter associated with antigen presentation; RIB, ribosome; PRO, proteasome.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 6
FIGURE 6

Age-specific prevalence of IgG antibodies against HCMV.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 7
FIGURE 7

CMV load in the urine of neonates. TCID, 50% tissue culture infective dose. Symbols: ◯, symptomatic congenital infection; •, asymptomatic; ■, natal infection. Error bars indicate standard errors of the means.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 8
FIGURE 8

CMV load in the urine of renal transplant recipients.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 9
FIGURE 9

Threshold concept of CMV pathogenesis.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 10
FIGURE 10

Histologic section of a lung sample from a patient with HCMV pneumonitis following bone marrow transplantation. Arrows show alveolar macrophages bearing the typical intranuclear inclusions of HCMV. An interstitial mononuclear cell infiltrate is seen.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 11
FIGURE 11

Histologic appearance of the inner ear in a patient with a fatal case of cytomegalic inclusion disease. Note the focus of large inclusion-bearing cells and accompanying inflammation. (Courtesy of S. Stagno. Reprinted from reference with permission.)

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 12
FIGURE 12

Correlation between high HCMV load and detection of intranuclear inclusions. ge, genomes.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 13
FIGURE 13

Photograph of human embryonic lung fibroblasts showing the focal CPE of HCMV. (Figure prepared by J. A. Bishop.)

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 16
FIGURE 16

Schematic representation of the UL97 gene showing mutations at particular codons that have been proven to cause resistance to ganciclovir or that are associated with maribavir resistance . Bold letters indicate mutations confirmed by site-directed mutagenesis. Mutations 460 to 607 refer to ganciclovir; mutations 353 to 411 refer to maribavir. (Data from reference .)

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 14
FIGURE 14

Herd immunity for HCMV or rubella ----, CMV study 1; ........, CMV study 2; - - - - - -, rubella.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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Image of FIGURE 15
FIGURE 15

Standard population models of susceptible, infectious, and immune individuals, modified to include seropositive individuals who act as a source of HCMV for reinfections.

Citation: Griffiths P, Reeves M. 2017. Cytomegalovirus, p 481-510. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch23
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