Congenital cytomegalovirus infection following first trimester maternal infection: Symptoms at birth and outcome

Pass, Robert F.; Fowler, Karen B.; Boppana, Suresh B.; Britt, William J.; Stagno, Sergio

doi:10.1016/j.jcv.2005.09.015

Cited by 416 publications

(300 citation statements)

References 26 publications

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“…Further evidence for the validity of our mouse model relates to the onset time of CMV infection. Human data shows an age-dependent effect such that children are more likely to develop hearing loss after maternal CMV infection during the first trimester than later in pregnancy (Pass et al 2006). By analogy, in our mouse model, all postnatal day 3 (P3) infected mice had elevated ABR thresholds at 4 weeks of age; of those inoculated at P8, only 15 % had ABR threshold shifts.…”

Section: Introductionmentioning

confidence: 63%

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: 63%

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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“…25 Pass et al also demonstrated, in a short retrospective study of infected newborns, that sensorineural hearing loss and sequelae were significantly more frequent in the first trimester than later. 26 Feldman described severely infected cases in the early second trimester but not later. 16 These results are in accordance with what is well known for other congenital infections (rubella or toxoplasmosis).…”

Section: Discussionmentioning

confidence: 99%

“…Each subject included had maternal primary CMV infection assessed by serology analysis and precise gestational dating. Subjects were classified in different subgroups according to the time of maternal infection: preconceptional (2 months to 3 weeks before the date of conception), periconceptional (3 weeks before to 3 weeks after the date of conception), or first (3-14 weeks of gestation [WG]), second (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) or third trimester of pregnancy (28 WG up to delivery). Subjects with imprecise date of maternal infection were excluded from the study.…”

Section: Methodsmentioning

confidence: 99%

A series of 238 cytomegalovirus primary infections during pregnancy: description and outcome

et al. 2013

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Objective To analyze the outcome of maternal primary cytomegalovirus (CMV) infection.Methods Retrospective analysis of a cohort of 238 patients with maternal primary CMV infection detected at routine screening. The cases were managed with serial ultrasound (US) scans, and amniocentesis was performed in 36.1% of cases. All prenatal results were confirmed at birth. ResultsThe average age was 31.9 (18-44) years. Patients were symptomatic in 21% of cases. The rate of intrauterine transmission was 24.9%, and it was 8.8%, 19%, 30.6%, 34.1% and 40% in the preconceptional period, the periconceptional period, and the first, second and third trimesters of pregnancy, respectively (p = 0.025). There was a significantly higher risk of US abnormalities when maternal infection occurred during the preconceptional or periconceptional period and the first trimester compared with later (p < 0.001). Because of US abnormalities, pregnancy was terminated in 18 cases at the parents' request. Three infected newborns were symptomatic; all three cases were suspected at US before birth. We did not observe any symptomatic fetal infection when maternal infection occurred after 14 weeks of gestation. A number of clinically asymptomatic cases (5.5%) developed hearing loss. ConclusionThe rate of materno fetal transmission is linearly correlated to the gestational age at infection. No severe case of congenital infection was observed if maternal infection occurred after 14 weeks of gestation.

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“…However, immunocompromised hosts (i.e., hematopoietic and organ transplant recipients, AIDS patients) are at risk for development of severe HCMV disease. HCMV is the leading cause of congenital infection in the developed world, and can result in mental retardation and deafness (2)(3)(4). In addition, HCMV has been related to the development of atherosclerosis and immunosenescence (5,6).…”

Section: H Uman CMV (Hcmv) Is a B-herpesvirus That Infects 40-mentioning

confidence: 99%

Antibody-Mediated Response of NKG2Cbright NK Cells against Human Cytomegalovirus

Costa‐García

Vera

Moraru³

et al. 2015

The Journal of Immunology

103

108

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Human CMV (HCMV) infection promotes a variable and persistent expansion of functionally mature NKG2Cbright NK cells. We analyzed NKG2Cbright NK cell responses triggered by Abs from HCMV+ sera against HCMV-infected MRC5 fibroblasts. Specific Abs promoted the degranulation (i.e., CD107a expression) and the production of cytokines (TNF-α and IFN-γ) by a significant fraction of NK cells, exceeding the low natural cytotoxicity against HCMV-infected targets. NK cell–mediated Ab-dependent cell-mediated cytotoxicity was limited by viral Ag availability and HLA class I expression on infected cells early postinfection and increased at late stages, overcoming viral immunoevasion strategies. Moreover, the presence of specific IgG triggered the activation of NK cells against Ab-opsonized cell-free HCMV virions. As compared with NKG2A+ NK cells, a significant proportion of NKG2Cbright NK cells was FcεR γ-chain defective and highly responsive to Ab-driven activation, being particularly efficient in the production of antiviral cytokines, mainly TNF-α. Remarkably, the expansion of NKG2Cbright NK cells in HCMV+ subjects was related to the overall magnitude of TNF-α and IFN-γ cytokine secretion upon Ab-dependent and -independent activation. We show the power and sensitivity of the anti-HCMV response resulting from the cooperation between specific Abs and the NKG2Cbright NK-cell subset. Furthermore, we disclose the proinflammatory potential of NKG2Cbright NK cells, a variable that could influence the individual responses to other pathogens and tumors.

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Congenital cytomegalovirus infection following first trimester maternal infection: Symptoms at birth and outcome

Cited by 416 publications

References 26 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

A series of 238 cytomegalovirus primary infections during pregnancy: description and outcome

Antibody-Mediated Response of NKG2Cbright NK Cells against Human Cytomegalovirus

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