Abstract
BackgroundCongenital cytomegalovirus (CMV) infection is the leading cause of sensorineural hearing loss (SNHL), and SNHL is the most frequent sequela of congenital CMV infection. But the pathogenic mechanism remains unknown, and there is no ideal CMV intrauterine infection animal model to study the mechanisms by which SNHL develops.MethodsWe established the congenital murine cytomegalovirus (MCMV) infection model by directly injecting the virus into the placenta on day 12.5 of gestation. Then, we observed the development and the MCMV congenital infection rate of the fetuses on the day they were born. Furthermore, we detected the auditory functions, the conditions of the MCMV infection, and the histological change of the inner ears of 28-day-old and 70-day-old offspring.ResultsBoth the fetal loss rate and the teratism rate of offspring whose placentas were inoculated with MCMV increased, and their body length, head circumference, and weight decreased. The hearing level of offspring both decreased at both 28- and 70-days post birth; the 70-day-old mice developed lower hearing levels than did the 28-day old mice. No significant inflammatory changes in the cochleae of the mice were observed. MCMV DNA signals were mainly detected in the spiral ganglion neurons and the endolymph area, but not in the perilymph area. The number of neurons decreased, and their ultrastructures changed. Moreover, with age, the number of neurons dramatically decreased, and the ultrastructural lesions of neurons became much more severe.ConclusionsThe results suggest that the direct injection of MCMV into the placenta may efficiently cause fetal infection and disturb the intrauterine development of the fetus, and placental inoculation itself has no obvious adverse effects on offspring. The reduction in the number of spiral ganglion neurons and the ultrastructural lesions of the neurons may be the major cause of congenital CMV infection-induced progressive SNHL.
Highlights
Congenital cytomegalovirus (CMV) infection is the leading cause of sensorineural hearing loss (SNHL), and SNHL is the most frequent sequela of congenital CMV infection
If a pregnant woman is infected with Human cytomegalovirus (HCMV), the virus can be transmitted through the placenta or cervix, causing intrauterine infection
At day 18.5 of gestation, viral DNA amplification using polymerase chain reaction (PCR) in the placenta was observed at 58.49% (31/53)
Summary
Congenital cytomegalovirus (CMV) infection is the leading cause of sensorineural hearing loss (SNHL), and SNHL is the most frequent sequela of congenital CMV infection. Human cytomegalovirus (HCMV) is the most common pathogen causing intrauterine infection in developing countries [1]. If a pregnant woman is infected with HCMV, the virus can be transmitted through the placenta or cervix, causing intrauterine infection. Approximately 40% to 58% of children with symptomatic infection and 13.5% of children with asymptomatic infection develop long-term neurological sequelae, including single- or two-sided progressive sensorineural hearing loss (SNHL), cognitive deficit, and motor deficit. Li et al [6] found that the intellectual development, especially the language skills development, of early childhood and preschool children with asymptomatic intrauterine HCMV infection is lower than that of normal children. The pure-tone threshold of preschool children with asymptomatic intrauterine HCMV infection is abnormal
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