Infectious Diseases Society of America and Centers for Disease Control: Summary of a Workshop on Surveillance for Congenital Cytomegalovirus Disease

Demmler, Gail J.

doi:10.1093/clinids/13.2.315

Cited by 442 publications

(166 citation statements)

References 101 publications

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“…In the USA, approximately 20,000 infants develop CMV infection annually; of these, 2000 are symptomatic at birth and suffer severe neurologic sequela. Approximately 18,000 are asymptomatic at birth but develop significant handicaps such as hearing impairment (Demmler 1991;Manicklal et al 2013). Quality of life and treatmentcost burdens are significant, and the development of new CMV vaccines is a high priority (Delany et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus (CMV) Infection Causes Degeneration of Cochlear Vasculature and Hearing Loss in a Mouse Model

Carraro

Almishaal

Hillas

et al. 2016

JARO

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Cytomegalovirus (CMV) infection is one of the most common causes of congenital hearing loss in children. We have used a murine model of CMV infection to reveal functional and structural cochlear pathogenesis. The cerebral cortex of Balb/c mice (Mus musculus) was inoculated with 2000 pfu (plaque forming units) of murine CMV on postnatal day 3. At 6 weeks of age, cochlear function was monitored using auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) measures. Histological assessment of cochlear vasculature using a corrosion cast technique was made at 8 weeks. Vascular casts of mCMV-damaged cochleas, and those of untreated control animals, were examined using scanning electron microscopy. We find very large variations in the degree of vascular damage in animals given identical viral injections (2000 pfu). The primary lesion caused by CMV infection is to the stria vascularis and to the adjacent spiral limbus capillary network. Capillary beds of the spiral ligament are generally less affected. The initial vascular damage is found in the mid-apical turn and appears to progress to more basal cochlear regions. After viral migration to the inner ear, the stria vascularis is the primary affected structure. We suggest that initial auditory threshold losses may relate to the poor development or maintenance of the endocochlear potential caused by strial dysfunction. Our increased understanding of the pathogenesis of CMV-related hearing loss is important for defining methods for early detection and treatment.

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Section: Introductionmentioning

confidence: 99%

Cytomegalovirus (CMV) Infection Causes Degeneration of Cochlear Vasculature and Hearing Loss in a Mouse Model

Carraro

Almishaal

Hillas

et al. 2016

JARO

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“…Among these, the eight members of the human herpesvirus family are the most frequent and significant causes of CNS infection; cytomegalovirus (CMV), for example, is the most commonly recognized cause of congenital anomalies of the human CNS (Stagno et al, 1986;Demmler, 1991;McCutchan, 1995;Mamidi et al, 2002). However, human herpesvirus (HHV) 6, the closest relative to CMV, is the most abundant resident HHV in the human brain, detectable in up to 70% of human brain tissues at autopsy (Sanders et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Infection with an Endemic Human Herpesvirus Disrupts Critical Glial Precursor Cell Properties

Dietrich¹,

Blumberg²,

Roshal³

et al. 2004

J. Neurosci.

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Human herpesvirus 6 (HHV-6), a common resident virus of the human CNS, has been implicated in both acute and chronic inflammatory-demyelinating diseases. Although HHV-6 persists within the human CNS and has been described to infect mature oligodendrocytes, nothing is known about the susceptibility of glial precursors, the ancestors of myelin-producing oligodendrocytes, to viral infection.We show that HHV-6 infects human glial precursor cells in vitro. Active infection was demonstrated by both electron microscopy and expression of viral gene transcripts and proteins, with subsequent formation of cell syncytia. Infection leads to alterations in cell morphology and impairment of cell replication but not increased cell death. Infected cells showed decreased proliferation as measured by bromodeoxyuridine uptake, which was confirmed by blunting of the cell growth rate of infected cells compared with uninfected controls over time. The detailed analysis using novel, fluorescent-labeled HHV-6A or HHV-6B reagents demonstrated strong G 1 /S phase inhibition in infected precursor cells. Cell cycle arrest in HHV-6-infected cells was associated with a profound decrease in the expression of the glial progenitor cell marker A2B5 and a corresponding increase in the oligodendrocyte differentiation marker GalC.These data demonstrate for the first time that infection of primary human glial precursor cells with a neurologically relevant human herpesvirus causes profound alterations of critical precursor cell properties. In light of recent observations that repair of CNS demyelination is dependent on the generation of mature oligodendrocytes from the glial precursor cell pool, these findings may have broad implications for both the ineffective repair seen in demyelinating diseases and the disruption of normal glial maturation.

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“…[2][3][4][5][6][7] Worldwide, cCMV infection affects 0.2% to 2.5% of all live-born neonates. [8][9][10][11] In industrialized countries, the average prevalence of cCMV infection is 0.64% to 0.70%. 4, 12 The incidence of cCMV infection is highest in developing countries, 1% to 5% of all live births, and is probably driven by nonprimary maternal infections.…”

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confidence: 99%

“…4,[33][34][35] The overall mortality rate is ,5%. 10,27,35,36 The majority of children with cCMV are asymptomatic and therefore not diagnosed at birth. However, 7% to 15% of clinically asymptomatic patients may develop late sequelae, including SNHL, which is by far the most common sequela.…”

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confidence: 99%

Hearing Loss and Congenital CMV Infection: A Systematic Review

Goderis¹,

Leenheer²,

et al. 2014

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BACKGROUND AND OBJECTIVE: Hearing loss caused by congenital cytomegalovirus (cCMV) infection was first observed in 1964. Today cCMV is the most common cause of nonhereditary sensorineural hearing loss in childhood. Our objective was to provide an overview of the prevalence of cCMV-related hearing loss, to better define the nature of cCMV-associated hearing loss, and to investigate the importance of cCMV infection in hearing-impaired children. METHODS:Two reviewers independently used Medline and manual searches of references from eligible studies and review articles to select cohort studies on children with cCMV infection with audiological follow-up and extracted data on population characteristics and hearing outcomes. RESULTS:Thirty-seven studies were included: 10 population-based natural history studies, 14 longitudinal cohort studies, and 13 retrospective studies. The prevalence of cCMV in developed countries is 0.58% (95% confidence interval, 0.41-0.79). Among these newborns 12.6% (95% confidence interval, 10.2-16.5) will experience hearing loss: 1 out of 3 symptomatic children and 1 out of 10 asymptomatic children. Among symptomatic children, the majority have bilateral loss; among asymptomatic children, unilateral loss predominates. In both groups the hearing loss is mainly severe to profound. Hearing loss can have a delayed onset, and it is unstable, with fluctuations and progression. Among hearing-impaired children, cCMV is the causative agent in 10% to 20%. Despite strict selection criteria, some heterogeneity was found between selected studies.CONCLUSIONS: This systematic review underscores the importance of cCMV as a cause of sensorineural hearing loss in childhood. Pediatrics 2014;134:972-982

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Infectious Diseases Society of America and Centers for Disease Control: Summary of a Workshop on Surveillance for Congenital Cytomegalovirus Disease

Cited by 442 publications

References 101 publications

Cytomegalovirus (CMV) Infection Causes Degeneration of Cochlear Vasculature and Hearing Loss in a Mouse Model

Cytomegalovirus (CMV) Infection Causes Degeneration of Cochlear Vasculature and Hearing Loss in a Mouse Model

Infection with an Endemic Human Herpesvirus Disrupts Critical Glial Precursor Cell Properties

Hearing Loss and Congenital CMV Infection: A Systematic Review

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