ArticleLaboratory investigation; a journal of technical methods and pathology2022
The S100A10-AnxA2 complex is associated with the exocytosis of hepatitis B virus in intrauterine infection.
Article in Laboratory investigation; a journal of technical methods and pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- ANXA2 in hepatocellular carcinoma: orchestrating tumorigenesis, progression, and therapeutic resistance toward precision targeting.Journal of translational medicine · 2025Review
- Mapping Small Extracellular Vesicle Secretion Potential in Healthy Human Gingiva Using Spatial Transcriptomics.Current issues in molecular biology · 2025Article
- Role of the Annexin A protein family in liver diseases: insights and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- Establishing a Multifaceted Comprehensive Maternity Cohort Facilitates Understanding of How Environmental Exposures Impact Perinatal Health.Environment & health (Washington, D.C.) · 2024Review
- Review
- Recent Advances in Molecular and Cellular Functions of S100A10.Biomolecules · 2023Review
- Intrauterine Infection and Mother-to-Child Transmission of Hepatitis B Virus: Route and Molecular Mechanism.Infection and drug resistance · 2022Review
- The Annexin A2/S100A10 Complex: The Mutualistic Symbiosis of Two Distinct Proteins.Biomolecules · 2021Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mother-to-child transmission (MTCT) is the major cause of chronic infection of hepatitis B virus (HBV) in patients. However, whether and how HBV crosses the placenta to cause infection in utero remains unclear. In this study, we investigate the mechanism as to how the HBV virions pass through layers of the trophoblast. Our data demonstrate the exocytosis of virions from the trophoblast after exposure to HBV where the endocytosed HBV virions co-localized with an S100A10/AnxA2 complex and LC3, an autophagosome membrane marker. Knockdown of either AnxA2 or S100A10 in trophoblast cells led to a reduction of the amount of exo-virus in Transwell assay. Immunohistochemistry also showed a high expression of AnxA2 and S100A10 in the placental tissue samples of HBV-infected mothers with congenital HBV-positive infants (HBV
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