Understanding the role of Newcastle disease virus-mediated cellular stress and altered proteostasis: Outsmarting the smart virus
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2025
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Abstract
Viruses are known to instigate a variety of stresses in their host cells, including endoplasmic reticulum (ER) and oxidative stress, to affect normal cell functioning and their replication cycle. The virus-induced stress subsequently triggers cellular stress responses by activating numerous stress-responsive proteins (SRPs). Afterward, all the viral proteins and SRPs substantially exacerbate ER protein flux, eliciting the unfolded protein response (UPR). This can be characterized by the modulation of Glucose-Regulated Protein 78 (GRP78) as an ER stress sensor. Moreover, viruses have also been shown to induce oxidative stress by disrupting the balance of reactive oxygen species (ROS) inside the cells. However, the purpose of virus-induced stresses and the precise role of SRPs in infection remain elusive. The present work utilizes the Newcastle disease virus (NDV) to investigate the role of cellular stress and the function of specific SRPs in pathogenesis.
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Supervisor: Kumar, Sachin