Cytomegalovirus infections during pregnancy

Nigro, Giovanni; Adler, Stuart P.

doi:10.1097/gco.0b013e328342f1f6

Cited by 55 publications

(60 citation statements)

References 43 publications

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“…CMV transmission in the first trimester is associated with the poorest fetal outcome [3]. Enders et al indicated that the rate of symptomatically infected fetuses or newborns at birth was 22.8 % for any symptoms and 10.3 % for severe manifestation, but no symptoms were observed in infected newborns of mothers with primary infection in the preconceptional period and the third trimester [7].…”

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

“…It is comprehensible that maternal preconceptional immunity against CMV gives relatively good protection to fetus, so a smaller proportion becomes infected. Preexisting humoral immunity protects seropositive pregnant women against CMV reinfection at a rate of 66-93 % [3]. The fetal outcome after congenital CMV infection is summarized in Figure 1.…”

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

“…Therefore, many symptoms of congenital CMV infection that are present at birth may not be due to any direct effect of the virus on the fetus but rather to the infection of placenta, which impairs its capacity to provide oxygen and nutrition to the developing fetus. Although not completely elucidated, placenta tissue damage is due to direct tissue injury by persistent CMV replication and immune complex deposition [3]. The increase in placental size occurs with primary maternal CMV infection, because the placental vasculature enlarges to compensate the fetus [8].…”

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

“…First, CMV causes both primary and recurrent maternal infection. Second, CMV is highly prevalent in both developed countries, where primary maternal infection is common, and developing countries, where recurrent infections are most common [3].…”

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

“…The burden of disease for congenitally infected infants includes intrauterine growth restriction, microcephaly, hepatosplenomegaly, petechiae, jaundice, chorioretinitis, thrombocytopenia, and anemia [2••]. In addition, congenital CMV infection can cause a variety of long-term disabilities, alone or in combination, such as mental retardation, learning disabilities, cerebral palsy, epilepsy, deafness or hearing impairment, and visual deficit or blindness [3].…”

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

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CMV Infection and Pregnancy

Tung

et al. 2012

Curr Obstet Gynecol Rep

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Cytomegalovirus (CMV) occurs in 0.2 % to 2.2 % of all live births and is the most common cause of intrauterine infection and the leading infectious cause of sensorineural hearing loss and mental retardation. This article reviews literature that relate to the pathogenesis, diagnosis, and treatment of this disease for pregnant women and their fetus. Primary maternal CMV infection during pregnancy has a much higher rate of mother-to-fetus transmission and causes symptoms at birth and long-term disability than nonprimary infection. In addition, some research has shown that children with congenital CMV infection following first-trimester maternal infection are more likely to have severe sequelae. The prenatal diagnosis of fetal CMV infection includes serological testing (IgM detection and IgG avidity assay), amniocentesis, and ultrasound examination. The combination of the presence of CMV IgM antibodies and low CMV IgG avidity, along with maternal or fetal symptoms is used for the diagnosis of a primary maternal infection. Amniocentesis should be complemented until approximately 20-21 weeks of gestation to increase the sensitivity. Because ultrasound abnormalities are only found in less than 25 % of infected fetuses, ultrasound is as a relatively poor predictor of symptomatic congenital infection. CMV hyperimmunoglobulin also may be considered when the pregnant women are confirmed as primary CMV infection with low IgG avidity and amniotic fluid is found to contain CMV or CMV DNA. There is no consensus on the benefit of prenatal administration of ganciclovir into the umbilical vein.

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Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

Section: Pathogenesis Of Congenital CMV Infectionmentioning

confidence: 99%

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CMV Infection and Pregnancy

Tung

et al. 2012

Curr Obstet Gynecol Rep

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Brain‐resident memory CD8⁺ T cells induced by congenital CMV infection prevent brain pathology and virus reactivation

et al. 2018

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Congenital HCMV infection is a leading infectious cause of long-term neurodevelopmental sequelae. Infection of newborn mice with mouse cytomegalovirus (MCMV) intraperitoneally is a well-established model of congenital human cytomegalovirus infection, which best recapitulates the hematogenous route of virus spread to brain and subsequent pathology. Here, we used this model to investigate the role, dynamics, and phenotype of CD8 T cells in the brain following infection of newborn mice. We show that CD8 T cells infiltrate the brain and form a pool of tissue-resident memory T cells (T cells) that persist for lifetime. Adoptively transferred virus-specific CD8 T cells provide protection against primary MCMV infection in newborn mice, reduce brain pathology, and remain in the brain as T cells. Brain CD8 T cells were long-lived, slowly proliferating cells able to respond to local challenge infection. Importantly, brain CD8 T cells controlled latent MCMV and their depletion resulted in virus reactivation and enhanced inflammation in brain.

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Frequent detection of human cytomegalovirus in neuroblastoma: A novel therapeutic target?

Wolmer-Solberg

Baryawno

Rahbar

et al. 2013

Intl Journal of Cancer

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Neuroblastoma is the most common and deadly tumor of childhood, where new therapy options for patients with high-risk disease are highly warranted. Human cytomegalovirus (HCMV) is prevalent in the human population and has recently been implicated in different cancer forms where it may provide mechanisms for oncogenic transformation, oncomodulation and tumor cell immune evasion. Here we show that the majority of primary neuroblastomas and neuroblastoma cell lines are infected with HCMV. Our analysis show that HCMV immediate-early protein was expressed in 100% of 36 primary neuroblastoma samples, and HCMV late protein was expressed in 92%. However, no infectious virus was detected in primary neuroblastoma tissue extracts. Remarkably, all six human neuroblastoma cell lines investigated contained CMV DNA and expressed HCMV proteins. HCMV proteins were expressed in neuroblastoma cells expressing the proposed stem cell markers CD133 and CD44. When engrafted into NMRI nu/nu mice, human neuroblastoma cells expressed HCMV DNA, RNA and proteins but did not produce infectious virus. The HCMV-specific antiviral drug valganciclovir significantly reduced viral protein expression and cell growth both in vitro and in vivo. These findings indicate that HCMV is important for the pathogenesis of neuroblastoma and that anti-viral therapy may be a novel adjuvant treatment option for children with neuroblastoma.

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Cytomegalovirus infections during pregnancy

Cited by 55 publications

References 43 publications

CMV Infection and Pregnancy

CMV Infection and Pregnancy

Brain‐resident memory CD8⁺ T cells induced by congenital CMV infection prevent brain pathology and virus reactivation

Frequent detection of human cytomegalovirus in neuroblastoma: A novel therapeutic target?

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Cytomegalovirus infections during pregnancy

Cited by 55 publications

References 43 publications

CMV Infection and Pregnancy

CMV Infection and Pregnancy

Brain‐resident memory CD8+ T cells induced by congenital CMV infection prevent brain pathology and virus reactivation

Frequent detection of human cytomegalovirus in neuroblastoma: A novel therapeutic target?

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Brain‐resident memory CD8⁺ T cells induced by congenital CMV infection prevent brain pathology and virus reactivation