On the basis of the sequence variation of the glycoprotein B (gB) gene, human cytomegalovirus (HCMV) can be classified into four gB genotypes. Genotyping of HCMV from congenital infections was carried out on the assumption that the envelope gB may influence the outcome of prenatal infection. Sixty-three pregnant women were included in the study: 40 pregnant women whose fetuses were strongly suspected of having viral infection, and 23 women with normal pregnancies, from whom amniotic fluid was taken for fetal karyotype assessment. The amniotic fluid, fetal blood, blood, and urine of the newborns were examined for HCMV DNA by a nested polymerase chain reaction, and the gB genotype was determined by restriction fragment length polymorphism. HCMV DNA was detected in 12 cases in which the fetuses were suspected of having a viral infection and in 3 of the normal pregnancies. All the HCMV DNA had identical genotype, gB1. These data clearly indicate the dominance of the gB1 genotype in congenital HCMV infections. The clinical outcome of these pregnancies, however, cannot be predicted on the basis of the involvement of this genotype.
On the basis of the sequence variation of the glycoprotein B (gB) gene, human cytomegalovirus (HCMV) can be classified into four gB genotypes. Genotyping of HCMV from congenital infections was carried out on the assumption that the envelope gB may influence the outcome of prenatal infection. Sixty-three pregnant women were included in the study: 40 pregnant women whose fetuses were strongly suspected of having viral infection, and 23 women with normal pregnancies, from whom amniotic fluid was taken for fetal karyotype assessment. The amniotic fluid, fetal blood, blood, and urine of the newborns were examined for HCMV DNA by a nested polymerase chain reaction, and the gB genotype was determined by restriction fragment length polymorphism. HCMV DNA was detected in 12 cases in which the fetuses were suspected of having a viral infection and in 3 of the normal pregnancies. All the HCMV DNA had identical genotype, gB1. These data clearly indicate the dominance of the gB1 genotype in congenital HCMV infections. The clinical outcome of these pregnancies, however, cannot be predicted on the basis of the involvement of this genotype.
Human cytomegalovirus (CMV) messenger (m) RNA expression in circulating leukocytes reflects directly viral activity in the human host. In this study, sixty-nine patients were monitored prospectively for CMV infection and mRNA expression during the first year after renal transplantation. Of the 69 recipients, 58 (84%) recipients were positive for CMV immediate early 1 (IE1) mRNA as detected by nucleic acid sequence-based amplification. The median onset of IE1 expression started at day 22 after transplantation and continued for a median duration of 82 days. IE1 mRNA expression started significantly earlier in recipients who developed an active CMV infection (P = 0.001) and in mycophenolate mofetil (MMF) treated recipients (P = 0.002). The duration of IE1 mRNA expression was significantly longer in recipients that had previously an early onset of IE1 mRNA expression (P = 0.001) and in recipients with active CMV infection (P = 0.007). Remarkably, longer prednisolone intake was correlated with a significantly (P = 0.02) shorter duration of IE1 expression compared to a longer duration of IE1 expression in recipients with only a short prednisolone intake. In recipients infected with glycoprotein B (gB) type 1 CMV strains, the duration of IE1 expression was significantly (P = 0.04) shorter compared to recipients infected with non-gB type 1 CMV strains (64 days vs. 150 days). The study indicates that multiple factors play a role in the onset and/or duration of CMV IE1 mRNA expression, for example, MMF treatment, prednisolone intake, and gB type of the specific CMV strain. The clinical significance of these correlations remains to be studied in more detail.
Congenital human cytomegalovirus (CMV) infection is the leading infectious cause of mental retardation, sensorineural deafness and visual impairment. It is mainly related to a primary maternal infection. The placenta should be considered the most important site of both the protection of the fetus from CMV infection and the transmission of CMV from mother to fetus. The control of the passage of CMV across the placenta probably involves a cascade of regulatory events. Roles are played by factors relating to the host immune-selective pressures, such as local cytokines and maternal CMV-specific neutralizing antibodies. The presence of other pathogens at the maternal-fetal interface also influences the outcome of CMV infection. Further investigations are needed in which clinical CMV strains are applied in in vitro studies to unravel the molecular mechanism of the intrauterine transmission of CMV and to elucidate the complex regulation that leads to prevention of the in utero transmission of CMV in vivo.
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