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© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Rubella infection (RuV) during early pregnancy is a known cause of congenital rubella syndrome (CRS). However, the mechanisms by which the virus crosses the placenta and infects the fetus are not fully understood. It has been known that various kinds of cell stresses can occur during the placenta formation. Previously, we demonstrated that low-glucose-induced endoplasmic reticulum stress could drastically enhance RuV infection in immortalized human first-trimester trophoblast cells. In this study, we investigated the roles of oxidative stress in RuV infection in these cells. Oxidative stress was induced in Swan.71 cells by culturing them in medium containing hydrogen peroxide (H2O2) in various concentrations and durations (50 µM or 100 µM for 24 h, or 150 µM for 1 h). RuV infection with a clinical strain was performed 24 h post-treatment, and capsid proteins were visualized at 24 and 48 h post-infection (hpi) using flow cytometry (FCM) and fluorescence microscopy (IF), respectively. The findings demonstrated that oxidative stress significantly enhanced RuV infection, as evidenced by FCM analysis, showing a twofold increase in infection rate, and confirmed by IF assay. Additionally, significantly increased intracellular viral replication was observed at 3 dpi. These findings suggest that oxidative stress during early pregnancy may promote the maternal-to-fetal transmission of rubella, contributing to the development of CRS.

Details

Title
Oxidative Stress Enhances Rubella Virus Infection in Immortalized Human First-Trimester Trophoblasts
Author
Trinh, Quang Duy 1   VIAFID ORCID Logo  ; Takada, Kazuhide 1   VIAFID ORCID Logo  ; Ngan Thi Kim Pham 2   VIAFID ORCID Logo  ; Takano, Chika 1   VIAFID ORCID Logo  ; Namiki, Takahiro 1   VIAFID ORCID Logo  ; Ito, Shun 1   VIAFID ORCID Logo  ; Takeda, Yoshinori 1 ; Okitsu, Shoko 1   VIAFID ORCID Logo  ; Ushijima, Hiroshi 1   VIAFID ORCID Logo  ; Hayakawa, Satoshi 1   VIAFID ORCID Logo  ; Komine-Aizawa, Shihoko 1   VIAFID ORCID Logo 

 Division of Microbiology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo 173-8610, Japan; [email protected] (K.T.); [email protected] (N.T.K.P.); [email protected] (C.T.); [email protected] (T.N.); [email protected] (S.I.); [email protected] (Y.T.); [email protected] (S.O.); [email protected] (H.U.); 
 Division of Microbiology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo 173-8610, Japan; [email protected] (K.T.); [email protected] (N.T.K.P.); [email protected] (C.T.); [email protected] (T.N.); [email protected] (S.I.); [email protected] (Y.T.); [email protected] (S.O.); [email protected] (H.U.); ; Department of Applied Molecular Chemistry, College of Industrial Technology, Nihon University, Chiba 274-0072, Japan 
First page
1041
Publication year
2025
Publication date
2025
Publisher
MDPI AG
ISSN
16616596
e-ISSN
14220067
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3165900529
Copyright
© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.