ArticleThe EMBO journal2024
Transplacental SARS-CoV-2 protein ORF8 binds to complement C1q to trigger fetal inflammation.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Mechanistic insights into the impact of prenatal viral infections on maternal and offspring immunity.Npj viruses · 2026Review
- SARS-CoV-2 ORF8: an accessory protein at the interface of immune evasion and inflammation.Frontiers in immunology · 2026Review
- CLL, together with C1qR, suppresses WSSV infection by regulating the activation of Dorsal.Journal of virology · 2025Article
- Joining the dots: maternal cytomegalovirus, HIV and the placenta.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- SARS-CoV-2 infection disrupts syncytial and endothelial integrity and alters PlGF levels in the placenta.Placenta · 2025Article
- Integrative genomic analysis identifies novel causal genes of Hodgkin's and non-Hodgkin's lymphoma.Discover oncology · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Prenatal SARS-CoV-2 infection is associated with higher rates of pregnancy and birth complications, despite that vertical transmission rates are thought to be low. Here, multi-omics analyses of human placental tissues, cord tissues/plasma, and amniotic fluid from 23 COVID-19 mother-infant pairs revealed robust inflammatory responses in both maternal and fetal compartments. Pronounced expression of complement proteins (C1q, C3, C3b, C4, C5) and inflammatory cytokines (TNF, IL-1α, and IL-17A/E) was detected in the fetal compartment of COVID-19-affected pregnancies. While ~26% of fetal tissues were positive for SARS-CoV-2 RNA, more than 60% of fetal tissues contained SARS-CoV-2 ORF8 proteins, suggesting transplacental transfer of this viral accessory protein. ORF8-positive fetal compartments exhibited increased inflammation and complement activation compared to ORF8-negative COVID-19 pregnancies. In human placental trophoblasts in vitro, exogenous ORF8 exposure resulted in complement activation and inflammatory responses. Co-immunoprecipitation analysis demonstrated that ORF8 binds to C1q specifically by interacting with a 15-peptide region on ORF8 (C37-A51) and the globular domain of C1q subunit A. In conclusion, an ORF8-C1q-dependent complement activation pathway was identified in COVID-19-affected pregnancies, likely contributing to fetal inflammation independently of fetal virus exposure.
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Registered trials
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