New Study Reveals Potential Link Between Maternal COVID-19 Infection and Neonatal Neurological Defects - medtigo



New Study Reveals Potential Link Between Maternal COVID-19 Infection and Neonatal Neurological Defects

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A recent study published by the American Academy of Pediatrics has reported potential long-term neurodevelopmental concerns for neonates following in-utero exposure to severe acute respiratory syndrome coronavirus disease 2 (SARS-CoV-2). The study presents the cases of two neonates born to SARS-CoV-2 positive mothers who displayed early-onset seizures, acquired microcephaly, and significant developmental delay over time.   

In Case 1, a preterm infant, neurologic findings included T2 hypointensity in the left germinal matrix and significant brain parenchyma atrophy. In Case 2, a term infant, there was an injury to the supratentorial cerebral cortex and severe bilateral cystic encephalomalacia. Upon brain pathology examination, Case 1 displayed reduced white matter volume, vacuolization, and hypoxia/ischemia. Furthermore, immunofluorescence images exhibited the presence of the SARS-CoV-2 virus in the brain.  

According to the study, neither infant was SARS-CoV-2 positive at birth, but both had detectable SARS-CoV-2 antibodies and increased blood inflammatory markers. Placentas from both mothers showed SARS-CoV-2-nucleocapsid protein and spiked glycoprotein 1 in the syncytiotrophoblast, fetal vascular malperfusion, and significantly increased inflammatory and oxidative stress markers. The neurologic findings at the birth of both infants mimicked the presentation of hypoxic-ischemic encephalopathy of a newborn, and neurologic sequelae progressed beyond the neonatal period.

Sequential MRI showed severe parenchymal atrophy and cystic encephalomalacia. One of the infants experienced sudden unexpected infant death at 13 months of age, and the deceased infant’s brain showed evidence of SARS-CoV-2. According to the research findings, maternal SARS-CoV-2 infection during the second trimester and placentitis could have instigated an inflammatory response and oxidative stress injury to the fetoplacental unit, thereby impacting the fetal brain. 

Moreover, the presence of SARS-CoV-2 in the brain of the deceased infant hints at the likelihood of direct fetal brain injury caused by the virus. The study found significant abnormalities in the placentas from both neonatal cases, indicating high-grade fetal vascular malperfusion. The fetal brain was affected by an inflammatory response and oxidative stress injury triggered by maternal SARS-CoV-2 infection during the second trimester with placentitis. 

The virus’s presence in the deceased infant’s brain suggests that it directly contributed to ongoing brain injury. The placental pathology also demonstrated increased HIF-1α, NLRP1, MIP-1β, SDF-1, IL-13, and IL-10, with a decreased hCG, indicating the virus’s presence. The study utilized Stochastic Optical Reconstruction Microscopy to perform immunofluorescence and detect the presence of SARS-CoV-2 spike glycoprotein 1 (S1) and nucleocapsid protein in the placenta and brain tissue of case-1 infant.

The results showed the presence of S1 in both case placentas, colocalized with the nucleocapsid protein of the syncytiotrophoblast. Furthermore, the study also found S1 protein and nucleocapsid protein throughout the brain of case 1. Both placentas of neonatal cases with maternal SARS-CoV-2 infection were compared with two SARS-CoV-2 negative mothers to detect possible inflammatory and modulating factors affecting fetal central nervous system development.

Immunofluorescence was used to identify hypoxia-inducible factor-α (HIF-α), Nucleotide-binding oligomerization domain and leucine-rich repeat-containing receptors pyrin domain containing one protein (NLRP1), macrophage inflammatory protein one β (MIP-1β), stromal cell-derived factor 1 (SDF1), interleukin 13, interleukin 10, and human chorionic gonadotropin (hCG). The study revealed elevated levels of HIF-1α, NLRP1, MIP-1β, SDF-1, IL-13, and IL-10, while hCG was markedly decreased.  


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