Congenital Cytomegalovirus Infection and Disease in Sweden and the Relative Importance of Primary and Secondary Maternal Infections: Preliminary Findings from a Prospective Study

Ahlfors, Karin; Ivarsson, Sten-Anders; Harris, Sten; Svanberg, L; Holmqvist, Rolf; Lernmark, Barbro; Theander, Georg

doi:10.3109/13813458409087131

Cited by 17 publications

(19 citation statements)

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“…As a result, viremia occurs as a rule only in primary infections (216), whereas it is either absent or undetectable in recurrent infections of the immunocompetent host (216) and common in recurrent infections of immunocompromised patients (67,137,147,179). Since, following primary HCMV infection, intrauterine transmission occurs in only 30 to 40% of cases, an innate barrier seems to partially prevent vertical transmission (4,50,110,264). In addition, a similar event seems to occur among infected newborns, less than 15% of whom show clinically apparent infection, in the great majority of cases resulting from primary maternal infection (4,50,75,264,293).…”

Section: Pathogenesis Of Congenital Infectionmentioning

confidence: 99%

“…Due to latency following primary infection and periodic reactivation of HCMV replication causing recurrent infections, in utero transmission of HCMV may follow either primary or recurrent infections (4,75,237,261,264). It is commonly recognized that primary HCMV infections are transmitted more frequently to the fetus and are more likely to cause fetal damage than recurrent infections (75).…”

Section: Epidemiology Of Vertical Hcmv Transmissionmentioning

confidence: 99%

“…Since, following primary HCMV infection, intrauterine transmission occurs in only 30 to 40% of cases, an innate barrier seems to partially prevent vertical transmission (4,50,110,264). In addition, a similar event seems to occur among infected newborns, less than 15% of whom show clinically apparent infection, in the great majority of cases resulting from primary maternal infection (4,50,75,264,293). Finally, in reactivated maternal infections, the risk of symptomatic congenital infection is even markedly lower (4,110,264), as shown by the few symptomatic infants reported in the past to have been born to mothers who were immune before pregnancy.…”

Section: Pathogenesis Of Congenital Infectionmentioning

confidence: 99%

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Diagnosis and Management of Human Cytomegalovirus Infection in the Mother, Fetus, and Newborn Infant

2002

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Human cytomegalovirus (HCMV) is the leading cause of congenital viral infection and mental retardation. HCMV infection, while causing asymptomatic infections in most immunocompetent subjects, can be transmitted during pregnancy from the mother with primary (and also recurrent) infection to the fetus. Hence, careful diagnosis of primary infection is required in the pregnant woman based on the most sensitive serologic assays (immunoglobulin M [IgM] and IgG avidity assays) and conventional virologic and molecular procedures for virus detection in blood. Maternal prognostic markers of fetal infection are still under investigation. If primary infection is diagnosed in a timely manner, prenatal diagnosis can be offered, including the search for virus and virus components in fetal blood and amniotic fluid, with fetal prognostic markers of HCMV disease still to be defined. However, the final step for definite diagnosis of congenital HCMV infection is detection of virus in the blood or urine in the first 1 to 2 weeks of life. To date, treatment of congenital infection with antiviral drugs is only palliative both prior to and after birth, whereas the only efficacious preventive measure seems to be the development of a safe and immunogenic vaccine, including recombinant, subunit, DNA, and peptide-based vaccines now under investigation. The following controversial issues are discussed in the light of the most recent advances in the field: the actual perception of the problem; universal serologic screening before pregnancy; the impact of correct counseling on decision making by the couple involved; the role of prenatal diagnosis in ascertaining transmission of virus to the fetus; the impact of preconceptional and periconceptional infections on the prevalence of congenital infection; and the prevalence of congenitally infected babies born to mothers who were immune prior to pregnancy compared to the number born to mothers undergoing primary infection during pregnancy

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Section: Pathogenesis Of Congenital Infectionmentioning

confidence: 99%

Section: Epidemiology Of Vertical Hcmv Transmissionmentioning

confidence: 99%

Section: Pathogenesis Of Congenital Infectionmentioning

confidence: 99%

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Diagnosis and Management of Human Cytomegalovirus Infection in the Mother, Fetus, and Newborn Infant

2002

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“…HCMV is an opportunistic pathogen, causing significant morbidity and mortality primarily in immunocompromised patients. Furthermore, transmission of HCMV to the fetus is the most common type of intrauterine infection (23,60), with a worldwide incidence of 0.5 to 2.2% (2,23,55). The fetus can be infected during all trimesters, in connection with either a primary or recurrent infection in the pregnant women (38,55).…”

mentioning

confidence: 99%

Human Cytomegalovirus Inhibits Neuronal Differentiation and Induces Apoptosis in Human Neural Precursor Cells

Odeberg

Wolmer

Falci

et al. 2006

J Virol

145

165

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Human cytomegalovirus (HCMV) is the most common cause of congenital infections in developed countries, with an incidence varying between 0.5 and 2.2% and consequences varying from asymptomatic infection to lethal conditions for the fetus. Infants that are asymptomatic at birth may still develop neurological sequelae, such as hearing loss and mental retardation, at a later age. Infection of neural stem and precursor cells by HCMV and consequent disruption of the proliferation, differentiation, and/or migration of these cells may be the primary mechanism underlying the development of brain abnormalities. In the present investigation, we demonstrate that human neural precursor cells (NPCs) are permissive for HCMV infection, by both the laboratory strain Towne and the clinical isolate TB40, resulting in 55% and 72% inhibition of induced differentiation of human NPCs into neurons, respectively, when infection occurred at the onset of differentiation. This repression of neuronal differentiation required active viral replication and involved the expression of late HCMV gene products. This capacity of HCMV to prevent neuronal differentiation declined within 24 h after initiation of differentiation. Furthermore, the rate of cell proliferation in infected cultures was attenuated. Surprisingly, HCMV-infected cells exhibited an elevated frequency of apoptosis at 7 days following the onset of differentiation, at which time approximately 50% of the cells were apoptotic at a multiplicity of infection of 10. These findings indicate that HCMV has the capacity to reduce the ability of human NPCs to differentiate into neurons, which may offer one explanation for the abnormalities in brain development associated with congenital HCMV infection.

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“…Other studies have shown that serious defects may result from infection in both early and late pregnancy. [6][7][8] Congenital infection may result from either primary or recurrent (due to reactivation of reinfection) infection in the mother. Although serious handicaps are more likely after primary rather than recurrent infection,219 neurological damage and bilateral hearing loss have occasionally been reported in children whose mothers undoubtedly had recurrent infection.2720 More data are required from large prospective studies before the risk associated with recurrent infection can be determined.…”

Section: Congenital Cytomegalovirus Infectionmentioning

confidence: 99%