Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
Cellular stress, induced by diverse factors including viral infection, reactive oxygen species (ROS), hypoxia, and toxin exposure, disrupts normal cellular function. The endoplasmic reticulum (ER) is pivotal in managing cellular stress, notably through the unfolded protein response (UPR) and ERas...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Pasteur Institute of Iran
2024-09-01
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| Series: | Journal of Medical Microbiology and Infectious Diseases |
| Subjects: | |
| Online Access: | https://jommid.pasteur.ac.ir/article-1-699-en.html |
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| Summary: | Cellular stress, induced by diverse factors including viral infection, reactive
oxygen species (ROS), hypoxia, and toxin exposure, disrupts normal cellular
function. The endoplasmic reticulum (ER) is pivotal in managing cellular
stress, notably through the unfolded protein response (UPR) and ERassociated
degradation (ERAD) pathways. This intricate process involves a
complex interplay of transcription factors and signaling molecules. During
viral infection, cells activate a multifaceted antiviral response, which is
specifically modulated by both the virus type and the molecular mechanisms
of the host's immune system. For instance, certain viruses like Japanese
encephalitis virus (JEV) exploit multiple cellular pathways for replication
and propagation. Viral infection can significantly impact cellular processes
like autophagy and apoptosis, either promoting or suppressing these
pathways. Thus, the cellular response to viral infection represents a dynamic
interplay that can either benefit the host or be exploited by the virus for its
propagation. For instance, viruses within the Flaviviridae family often
preserve host cell viability during early infection to enhance replication,
subsequently triggering apoptosis or other cell death mechanisms to
facilitate viral dissemination. This review explores the diverse responses of
infected cells to various viruses, highlighting the complex molecular
strategies employed by both host and pathogen. |
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| ISSN: | 2345-5349 2345-5330 |