Rubella virus infection in endothelial cells reduces angiogenesis via interferon beta-induced CXCL10.
Immunology
Virology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
21 Apr 2023
21 Apr 2023
Historique:
received:
05
12
2022
revised:
12
01
2023
accepted:
03
03
2023
medline:
4
4
2023
entrez:
3
4
2023
pubmed:
4
4
2023
Statut:
epublish
Résumé
Rubella virus (RuV) infection during pregnancy can lead to abortion, stillbirth, and embryonic defects, resulting in congenital rubella syndrome (CRS). It is estimated that there are still 100,000 cases of CRS per year in developing regions with a mortality rate of over 30%. The molecular pathomechanisms remain largely unexplored. Placental endothelial cells (EC) are frequently infected with RuV. RuV reduced the angiogenic and migratory capacity of primary human EC, as confirmed by treatment of EC with serum from RuV IgM-positive patients. Next generation sequencing analysis revealed the induction of antiviral interferon (IFN) type I and III and CXCL10. The RuV-induced transcriptional profile resembled the effects of IFN-β treatment. The RuV-mediated inhibition of angiogenesis was reversed by treatment with blocking and neutralizing antibodies targeting CXCL10 and the IFN-β receptor. The data identify an important role for antiviral IFN-mediated induction of CXCL10 in the control of EC function during RuV infection.
Identifiants
pubmed: 37009214
doi: 10.1016/j.isci.2023.106352
pii: S2589-0042(23)00429-7
pmc: PMC10060672
doi:
Types de publication
Journal Article
Langues
eng
Pagination
106352Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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