Placentas from SARS-CoV-2 infection during pregnancy exhibit foci of oxidative stress and DNA damage
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Problem
COVID-19 during pregnancy is linked to increased maternal morbidity and a higher incidence of preterm births, yet the underlying mechanisms remain unclear. Cellular senescence, characterized by the irreversible cessation of cell division, is a critical process in placental function and its dysregulation has been implicated in pregnancy complications like preterm birth. Senescence can be induced by various stressors, including oxidative stress, DNA damage, and viral infections.
Method of Study
In this study, we determined whether COVID-19 had an impact on placental senescence. We examined placentas from women infected with SARS-CoV-2 (n=10 term, 4 preterm) compared to uninfected controls (n=10 term, 3 preterm). The placentas were analyzed for SARS-CoV-2 infection/replication (Spike and Nucleocapsid viral proteins), markers of DNA damage (γH2AX) and oxidative stress (ROS), and senescence (telomere length; cell cycle regulators, SASP).
Results
While no overall differences in cellular senescence markers were observed between the COVID-19 positive and negative groups, we found increased secreted SASP markers and confocal microscopy revealed localized areas of oxidative stress and DNA damage in the placentas from COVID-19 positive cases.
Conclusions
These findings indicate that SARS-CoV-2 infection induces localized placental damage, warranting further investigation into its impact on maternal and perinatal outcomes.
