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.