Fetal inflammatory response and endothelial dysfunction in newborns from mothers with exacerbation of cytomegalovirus infection during the second trimester of pregnancy
Authors: Gorikov I. N. 
Published: April 2022

Aim. To study the fetal inflammatory response and endothelial dysfunction in newborns from mothers with an exacerbation of cytomegalovirus infection (CMVI) in the second trimester of pregnancy.

   Materials and methods. We examined 90 newborns with an antenatal history, uncomplicated and aggravated by the acute phase of chronic CMVI, diagnosed in their mothers at 21-24 weeks of gestation. The concentration of TNFα, IL-6, and endothelin-1 was determined in cord blood serum. The control group consisted of 30 newborns whose intrauterine development proceeded against the background of physiological pregnancy seronegative for cytomegalovirus (CMV). The main group included 60 newborns, which were divided into 2 subgroups. Subgroup 1 included 30 newborns from mothers who had an acute phase of chronic CMVI, leading to the development of chronic compensated placental insufficiency, subgroup 2 consisted of 30 newborns from mothers with exacerbation of CMVI, initiating the formation of chronic subcompensated placental insufficiency.

   Results. In the control group, DNA of CMV, IgM antibodies to CMV and IgG antibodies to CMV were not detected. In the main group, in newborns of subgroup 1, compared with the control, DNA of CMV, both in the cord blood and in the nasopharyngeal aspirate, was isolated in 3.3 % of cases, and was not detected in scrapings of the buccal epithelium. The titers of IgG antibodies to CMV were determined in the ratio of 1: 100 in 36.7 %, 1: 200 in 43.3 %, 1: 400 in 13.3% and 1: 800 in 6.7 % of cases. At the same time, in mother-newborn pairs, higher titers of IgG antibodies to CMV in pregnant women, compared with those in their offspring, were detected in 18 cases, and equal titers of IgG antibodies to CMV were detected in 12 dyads. In the control group, the concentration of TNFα was equal to (Me) 16.2 (12.9-32.7) pg/ml, IL-6 – 1.93 (1.65-2.21) pg/mL, endothelin-1 – 0.52 (0.45–1.21) fmol/mL. In subgroup 1 of the main group, in comparison with the control one, there was an increase in the concentration of TNFα by 2.6 times (p=0.000001), IL-6 – by 2.1 times (p = 0.000001) and endothelin-1 – by 2.1 time (p = 0.000002). In newborns of subgroup 2, compared with subgroup 1, CMV antigens were identified in the blood in 6.7 % (p > 0.05), and in nasopharyngeal aspirate – in 10% (p>0.05) in the absence of identification of the CMV genome in the buccal epithelium. In 6.7%, IgM antibodies to CMV were detected. IgG antibodies to CMV 1:800 were detected more often (in 33.3%, p<0.05), as well as equal titers of IgG antibodies to CMV in 20 mother-offspring pairs (p<0.05). There was an increase in the concentration of TNFα by 1.47 times (p=0.0076), IL-6 - by 1.33 (p = 0.0016) and endothelin-1 - by 1.5 times (p = 0.0161), respectively.

   Conclusion. In the offspring of mothers who had an exacerbation of CMVI in the second trimester of pregnancy and with the presence of chronic subcompensated placental insufficiency, compared with newborns from women with the acute phase of chronic CMVI at similar gestation periods and formed chronic compensated placental insufficiency, higher levels of pro-inflammatory cytokines and endothelin-1 are recorded, indicating activation of the fetal immune system as a result of viral aggression and penetration of IgG to CMV of maternal origin.