# TBSV Alters Host Redox State After Short-Term Temperature Pre-Exposure in Nicotiana benthamiana

## TL;DR

This study shows how prior temperature stress affects plant redox balance and influences Tomato bushy stunt virus infection in Nicotiana benthamiana.

## Contribution

The study reveals how prior heat or cold stress alters the host's redox state and modulates Tomato bushy stunt virus infection.

## Key findings

- TBSV infection increases hydrogen peroxide but decreases superoxide in infected plants.
- Heat pre-exposure increases lipid peroxidation, which is further reduced after infection.
- Infection and thermal stress both increase oxidative DNA damage and alter 8-oxoguanine glycosylase levels.

## Abstract

Plant viruses can cause substantial yield losses, yet disease severity often varies between seasons because plants frequently experience heat or cold episodes before infection. In this study, we tested whether such temperature conditions affect the plant’s redox balance and alter its response to Tomato bushy stunt virus (TBSV) infection in Nicotiana benthamiana. Plants were exposed to short-term heat and cold stress, after which they recovered before virus inoculation. Following this, we assessed the reactive oxygen species (ROS) content, lipid peroxidation (LPO), oxidative DNA damage, stress-related proteins, redox-associated enzymes, and antioxidant metabolites. TBSV led to non-parallel ROS responses during infection, with consistently elevated hydrogen peroxide in infected plants but reduced superoxide relative to corresponding mock controls. Heat pre-exposure caused pronounced LPO that decreased further after infection, whereas cold pre-exposure stabilized malondialdehyde near levels observed at 25 °C. Both thermal stress and infection increased 8-oxo-dG and were associated with distinct changes in 8-oxoguanine glycosylase abundance. Infection strongly induced heat shock protein 90 (and moderately heat shock protein 70), while prior heat limited further chaperone induction by TBSV. These results indicate that viral infection develops within and is limited by the host’s oxidative state, where redox homeostasis may restrict infection-related processes, and infection leads to changes in this redox environment that are favorable for its development.