It’s estimated that in the United States of America almost 50 million people are infected with this type of computer virus [37]. the order of the contamination, main or reinfection or chronic, the duration of membrane rupture, type of delivery, socio-economic conditions and breastfeeding. Frequently infected neonates, symptomatic at birth, have worse outcomes than asymptomatic. Many asymptomatic babies develop long term neurosensory outcomes. The way in which the computer virus interacts with the maternal immune system, the maternal-fetal interface and the placenta explain these results and also the differences that are observed from time to time in the fetal?neonatal outcomes of maternal infections. The maternal immune system undergoes functional adaptation during pregnancy, once thought as physiological immunosuppression. This adaptation, crucial for generating a balance between maternal immunity and fetus, is necessary to promote and support the pregnancy itself and the growth of the fetus. When this adaptation is upset by the viral contamination, the balance is usually broken, and the contamination can spread and lead to the adverse outcomes previously described. In this review we will describe the main viral harmful infections in pregnancy and the potential mechanisms of the damages around the fetus and newborn. Keywords: Cytomegalovirus, Herpes simplex 1-2, Herpes virus 6, Hepatitis B, Hepatitis C, HIV, Parvovirus B19, Enterovirus, Varicella, SARS-Cov-2, Zika, Fetuses, Neonates 1.?Introduction Some maternal infections, contracted before or during pregnancy, can be transmitted to the fetus, during gestation (congenital contamination), during labor and childbirth (perinatal contamination) and through breastfeeding (postnatal contamination). The brokers responsible for these infections can be viruses, bacteria, protozoa, fungi. Among the viruses most frequently responsible for congenital infections are Cytomegalovirus (CMV), Herpes simplex 1-2 (HSV 1-2), Herpes virus 6 (HHV-6), Varicella zoster computer virus (VZV), Rubella computer virus (RuV). Moreover, Hepatitis B and C computer virus (HBV and HCV), Human immunodeficiency computer virus (HIV), Parvovirus B19 (B19V) and non-polio Enterovirus (EV) when contracted during pregnancy may involve the fetus or newborn at birth. Recently, new viruses have emerged, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Zika computer virus (ZIKV), of which we do not yet fully know the characteristics and pathogenic power when contracted during pregnancy. In this review we will describe the main viral harmful infections in pregnancy and the potential mechanisms of the damages around the fetus and newborn (Fig. 1 ). Open in a separate windows Fig. 1 Summary of the potential injuries of viral Emeramide (BDTH2) infections during pregnancy. 2.?Search strategy and selection criteria We searched PubMed using the name of the considered computer virus (CMV, HSV 1-2, HHV-6, VZV, RuV, HBV, HCV, HIV, B19V, EV, SARS-CoV-2 and ZIKV) in combination with one of the following terms: subfamily of family. Congenital CMV Emeramide (BDTH2) contamination, more frequent in cases of poor socioeconomic status [1], may have serious clinical effects [2,3]. Considering the relatively high number of CMV seronegative women of reproductive age, the risk of main CMV contamination during gestation is relevant [4]. Moreover, unlike other infectious diseases, the risk of fetal involvement from CMV contamination in pregnancy is usually greater in the population, as the prevalence of serological positivity in women of childbearing age is usually high. CMV after a first contamination can cause reactivations in the pregnant woman, being able to determine fetal contamination [5]. In this last situation the probability of CMV transmission to the fetus is lower than in the course of the first maternal contamination. The transplacental transmission of human CMV contamination during pregnancy is about 20C70% during the Emeramide (BDTH2) main maternal infections, whilst the risk of Sparcl1 transmission/disease is lower as 1C1,5% in case of recurrent contamination [6]. Transmission may occur throughout the whole pregnancy period, but mainly in the first trimester [7], coming into contact with body fluids (such as saliva, urine, blood, and genital secretions) from an infected individual. 10C15% of infected neonates become symptomatic early after birth. Emeramide (BDTH2) Symptoms of CMV contamination detectable already at birth include intrauterine growth retardation (IUGR), purpura, jaundice, hepatosplenomegaly, microcephaly, hearing impairment, and thrombocytopenia [8]. About 40C60% of cases symptomatic at birth subsequently develop long-term sequelae (neurological disorders, vision and hear loss) [2,3]. In contrast, child years sequelae developing after an asymptomatic early postnatal period occur in 10C15% of cases, and mostly include progressive hearing loss [9]. 2) Mechanisms of fetal damage A proper understanding of the pathogenetic mechanisms leading to intrauterine CMV contamination is usually auspicable to optimize the prophylactic and/or therapeutic interventions and improve the outcome of the affected children. However, such underlying mechanisms are not completely obvious yet [10]. A key issue emerged in the last years is the key role of placental.