scholarly journals Isolated Temporal Lobes T2 Hyperintensity on Fetal MRI does not Predict Congenital CMV Infection

Author(s):  
Larisa Gorenstein
2016 ◽  
Vol 44 (3) ◽  
Author(s):  
Eran Hadar ◽  
Liat Salzer ◽  
Elizabeta Dorfman ◽  
Jacob Amir ◽  
Joseph Pardo

AbstractThis study aimed to evaluate antenatal risk factors associated with symptomatic congenital cytomegalovirus (CMV) disease, followingThis study included a retrospective cohort of 155 neonates with congenital CMV infection, following primary maternal CMV infection during pregnancy, and were divided to symptomatic (n=95) and asymptomatic (n=60) newborns.Young maternal age (29.1±5.12 vs. 31.6±5.36 years, P=0.005), high risk occupation for viral exposure (20.0% vs. 11.7%, P=0.04), CMV IgG seroconversion at diagnosis (83.1% vs. 63.3%, P=0.005) and abnormal fetal MRI (11.6% vs. 0%, P=0.003) were found to be prognostic risk factors associated with symptomatic CMV disease of the newborn. Maternal febrile illness at diagnosis, IgG avidity, US findings and the timing of maternal infection were not associated with the occurrence of neonatal symptoms.Knowledge of the reported risk factors may assist in counseling parents with intra uterine CMV infection.


2021 ◽  
Vol 17 (6) ◽  
pp. 51-56
Author(s):  
D.V. Maltsev ◽  
L.I. Melnik ◽  
I.A. Maltseva

Congenital CMV infection is thought to occur in at least 1 % of infants, although recent clinical studies indicate that these lesions account for 8 % of all neonates. The severity of clinical symptoms of nervous system damage of CMV-etiology depends on the duration of intrauterine infection. In early infection, during the first trimester of the fetal period, severe CNS malformations develop, including anencephaly, porencephaly, schizencephaly, lissencephaly, micropolygyria, and pachygyria. At later infection, during the 2nd–3rd trimesters of pregnancy, there are milder manifestations — ventriculomegaly, impaired myelination of the white matter of the brain, cysts in the poles of the temporal lobes, hypogenesis of the corpus callosum, periventricular calcifications, and lesions of the cochleovestibular nerves. The article presents the medical history of a 5-year-old boy with typical clinical and instrumental signs of congenital CMV infection. The child had deep spastic tetraparesis, severe mental retardation, refractory epileptic syndrome with polymorphic seizures, disorders of pelvic organs, inability to move independently. MRI of the brain showed typical radiological signs of congenital CMV infection: cortical atrophy, ventriculomegaly, periventricular gliosis, demyelination fields in the white matter of the hemispheres, cysts in the poles of the temporal lobes, hypoplasia of the corpus callosum. During the neonatal period, specific IgM to CMV in serum was observed. Blood leukocyte PCR revealed the CMV DNA in a 5-year-old child at the time of admission to the clinic. This infection led to genera-lized lymphadenopathy, hepatosplenomegaly, thrombocytopenia, and lymphomonocytosis. The assessment of immune status showed the presence of selective IgA deficiency, which was associated with the development of this opportunistic infection. Typical mistakes in the clinical management of children with congenital CMV infection and ways to avoid them are discussed.


2021 ◽  
Vol 138 ◽  
pp. 104793
Author(s):  
Justine Demortier ◽  
Jacques Fourgeaud ◽  
Soumeth Abasse ◽  
Laurent Lambrecht ◽  
Marie Gromand ◽  
...  

Author(s):  
E. Walter ◽  
C. Brennig ◽  
V. Schöllbauer ◽  
Gabriele Halwachs-Baumann

2006 ◽  
Vol 28 (4) ◽  
pp. 423-423
Author(s):  
G. Simonazzi ◽  
B. Guerra ◽  
A. Banfi ◽  
G. Pilu ◽  
T. Lazzarotto ◽  
...  

Retrovirology ◽  
2009 ◽  
Vol 6 (Suppl 1) ◽  
pp. O12
Author(s):  
Marianne Leruez-Ville ◽  
Christelle Vauloup-Fellous ◽  
Sophie Couderc ◽  
Sophie Parat ◽  
Salima Oucherif ◽  
...  

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1467
Author(s):  
K. Yeon Choi ◽  
Alistair McGregor

A vaccine against congenital cytomegalovirus infection is a high priority. Guinea pig cytomegalovirus (GPCMV) is the only congenital CMV small animal model. GPCMV encodes essential glycoprotein complexes for virus entry (gB, gH/gL/gO, gM/gN) including a pentamer complex (gH/gL/GP129/GP131/GP133 or PC) for endocytic cell entry. The cohorts for protection against congenital CMV are poorly defined. Neutralizing antibodies to the viral glycoprotein complexes are potentially more important than an immunodominant T-cell response to the pp65 protein. In GPCMV, GP83 (pp65 homolog) is an evasion factor, and the GP83 mutant GPCMV has increased sensitivity to type I interferon. Although GP83 induces a cell-mediated response, a GP83-only-based vaccine strategy has limited efficacy. GPCMV attenuation via GP83 null deletion mutant in glycoprotein PC positive or negative virus was evaluated as live-attenuated vaccine strains (GP83dPC+/PC-). Vaccinated animals induced antibodies to viral glycoprotein complexes, and PC+ vaccinated animals had sterilizing immunity against wtGPCMV challenge. In a pre-conception vaccine (GP83dPC+) study, dams challenged mid-2nd trimester with wtGPCMV had complete protection against congenital CMV infection without detectable virus in pups. An unvaccinated control group had 80% pup transmission rate. Overall, gB and PC antibodies are key for protection against congenital CMV infection, but a response to pp65 is not strictly necessary.


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