Main findings
CMV DNA was found in 5.2% of maternal and 5.4% of fetal interface.
Many studies have reported that the presence of CMV in the amniotic
fluid and placenta may be transient, but it is known that various cell
types present in placenta have receptors for the virus and, therefore,
are permissive to the infection 1, 2,10. Avanzi et al.
(2013) demonstrated the total cellular permittivity for CMV infection
using in vitro cultures of placental mesenchymal cells, raising
evidence that the placenta is an important fetus contamination route by
the virus 11, and this correlation was previously
reported by other authors1,12-15. Kumazaki and
co-workers (2002) investigated biopsies from placental parenchyma and
membrane and were able to determine by PCR that CMV DNA may be present
on both maternal interface and villi, indicating that the virus may
persist in placental tissue independent of fetal infection4. The CMV prevalence is significant according to
studies that investigated CMV DNA presence by PCR in placentas
associated with fetal death, low birth weight and fetal hydrops,
resulting in a prevalence of 4% to 27.4% 2, 14 - 18.
Previously conflicting CMV prevalence data have been currently observed
along the last decades 4, 14 - 17.
Considering the high antibody prevalence in Brazilian population, with
90 to 95% women in fertile age, it was expected that a reactivation of
infection would indeed occur induced by virus replication and permanence
in placental tissue with or without infected cord blood, suggesting that
placental infection is more common than neonatal
disease14, 17. Theiler and co-workers (2006) have
found the presence CMV DNA in the cord blood from two out of 433
neonates by PCR assay, and one of those was asymptomatic for the
disease. Both were newborns from mothers presenting a profile of viral
reactivation (IgM negative/IgG positive) 22. Another
study compared samples from 983 women resulting in a risk profile of 9%
(maternal IgM seropositive) and CMV DNA prevalence of 0.4% in cord
blood 23. More recently, Uematsu and colleagues (2016)
investigated suspicious congenital asymptomatic CMV cases in 182
patients presenting neurological symptoms, 32,4ยจ% (54) were positive
for the infection at different levels of severity, demonstrating that
the infection effects may be latter observed, once that at the moment of
birth the newborns were not diagnosed 23. Albano and
co-workers (2017) reported CMV DNA prevalence in cord blood of donors
and revealed 59 congenital positive infection asymptomatic cases from
which only three mothers were diagnosed with CMV during gestation period25.
In this study, low weight and prematurity occurred in some newborns. Was
evident that some of the women presented infections during gestation
period, such as tuberculosis or urinary infection, and even there was a
case of HIV seropositive. The correlation between polimicrobiane
infections during gestation and maternal response modulation was
previously described, therefore demonstrating the course of infection
and closure of such situation26. There is the
possibility of CMV reactivation at any site once it is a classic
opportunist agent 21.