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Viral Infections and Their Ability to Modulate Endoplasmic Reticulum Stress Response Pathways.

Authors :
da Fonseca, Flávio Guimarães
Serufo, Ângela Vieira
Leão, Thiago Lima
Lourenço, Karine Lima
Source :
Viruses (1999-4915). Oct2024, Vol. 16 Issue 10, p1555. 12p.
Publication Year :
2024

Abstract

In eukaryotic cells, the endoplasmic reticulum is particularly important in post-translational modification of proteins before they are released extracellularly or sent to another endomembrane system. The correct three-dimensional folding of most proteins occurs in the ER lumen, which has an oxidative environment that is essential for the formation of disulfide bridges, which are important in maintaining protein structure. The ER is a versatile organelle that ensures the correct structure of proteins and is essential in the synthesis of lipids and sterols, in addition to offering support in the maintenance of intracellular calcium. Consequently, the cells needed to respond to demands caused by physiological conditions and pathological disturbances in the organelle homeostasis, leading to proper functioning of the cell or even programmed cell death. Disturbances to the ER function trigger a response to the accumulation of unfolded or misfolded proteins, known as the unfolded protein response. Such disturbances include abiotic stress, pharmacological agents, and intracellular pathogens, such as viruses. When misfolded proteins accumulate in the ER, they can undergo ubiquitination and proteasomal degradation through components of the ER-associated degradation system. Once a prolonged activity of the UPR pathway occurs, indicating that homeostasis cannot be reestablished, components of this pathway induce cell death by apoptosis. Here, we discuss how viruses have evolved ways to counteract UPR responses to maximize replication. This evolutionary viral ability is important to understand cell pathology and should be taken into account when designing therapeutic interventions and vaccines. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
19994915
Volume :
16
Issue :
10
Database :
Academic Search Index
Journal :
Viruses (1999-4915)
Publication Type :
Academic Journal
Accession number :
180485810
Full Text :
https://doi.org/10.3390/v16101555