Premium
Mechanisms and evidence of vertical transmission of infections in pregnancy including SARS‐CoV ‐2s
Author(s) -
Mahyuddin Aniza P.,
Kanneganti Abhiram,
Wong Jeslyn J.L.,
Dimri Pooja S.,
Su Lin L.,
Biswas Arijit,
Illanes Sebastian E.,
Mattar Citra N. Z.,
Huang Ruby Y.J.,
Choolani Mahesh
Publication year - 2020
Publication title -
prenatal diagnosis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.956
H-Index - 97
eISSN - 1097-0223
pISSN - 0197-3851
DOI - 10.1002/pd.5765
Subject(s) - covid-19 , transmission (telecommunications) , betacoronavirus , pregnancy , medicine , coronavirus infections , obstetrics , sars virus , virology , biology , computer science , telecommunications , infectious disease (medical specialty) , genetics , disease , outbreak
There remain unanswered questions concerning mother‐to‐child‐transmission of SARS‐CoV‐2. Despite reports of neonatal COVID‐19, SARS‐CoV‐2 has not been consistently isolated in perinatal samples, thus definitive proof of transplacental infection is still lacking. To address these questions, we assessed investigative tools used to confirm maternal‐fetal infection and known protective mechanisms of the placental barrier that prevent transplacental pathogen migration. Forty studies of COVID‐19 pregnancies reviewed suggest a lack of consensus on diagnostic strategy for congenital infection. Although real‐time polymerase chain reaction of neonatal swabs was universally performed, a wide range of clinical samples was screened including vaginal secretions (22.5%), amniotic fluid (35%), breast milk (22.5%) and umbilical cord blood. Neonatal COVID‐19 was reported in eight studies, two of which were based on the detection of SARS‐CoV‐2 IgM in neonatal blood. Histological examination demonstrated sparse viral particles, vascular malperfusion and inflammation in the placenta from pregnant women with COVID‐19. The paucity of placental co‐expression of ACE‐2 and TMPRSS2, two receptors involved in cytoplasmic entry of SARS‐CoV‐2, may explain its relative insensitivity to transplacental infection. Viral interactions may utilise membrane receptors other than ACE‐2 thus, tissue susceptibility may be broader than currently known. Further spatial‐temporal studies are needed to determine the true potential for transplacental migration.