Oxidative Stress Enhances Rubella Virus Infection in Immortalized Human First-Trimester Trophoblasts

Area of Science:

• Obstetrics and Gynecology
• Virology
• Cell Biology

Background:

• Rubella virus (RuV) infection in early pregnancy causes congenital rubella syndrome (CRS).
• Mechanisms of placental transmission and fetal infection by RuV remain unclear.
• Cellular stresses, including endoplasmic reticulum stress, can influence RuV infection.

Purpose of the Study:

• To investigate the role of oxidative stress in RuV infection of human first-trimester trophoblast cells.
• To determine if oxidative stress enhances RuV entry and replication in placental cells.

Main Methods:

• Swan.71 trophoblast cells were exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
• Cells were infected with a clinical RuV strain.
• Infection rates were quantified using flow cytometry (FCM) and fluorescence microscopy (IF).
• Intracellular viral replication was assessed at 3 days post-infection (dpi).

Main Results:

• Oxidative stress significantly increased RuV infection rates by twofold, confirmed by FCM and IF.
• Significantly enhanced intracellular viral replication was observed at 3 dpi.
• These results indicate oxidative stress promotes RuV infection in placental cells.

Conclusions:

• Oxidative stress enhances rubella virus infection and replication in human trophoblast cells.
• This suggests oxidative stress during early pregnancy could facilitate maternal-to-fetal RuV transmission.
• Findings contribute to understanding CRS pathogenesis and may inform prevention strategies.