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...

Full description

Saved in:
Bibliographic Details
Main Authors: Farzaneh Sheikholeslami1*, Reza Shirzad1, Fatemeh Motevalli2
Format: Article
Language:English
Published: Pasteur Institute of Iran 2024-09-01
Series:Journal of Medical Microbiology and Infectious Diseases
Subjects:
Online Access:https://jommid.pasteur.ac.ir/article-1-699-en.html
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850274052776656896
author Farzaneh Sheikholeslami1*
Reza Shirzad1
Fatemeh Motevalli2
author_facet Farzaneh Sheikholeslami1*
Reza Shirzad1
Fatemeh Motevalli2
author_sort Farzaneh Sheikholeslami1*
collection DOAJ
description 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.
format Article
id doaj-art-4c251d6b70aa43ea9819dd4a55c9fefd
institution OA Journals
issn 2345-5349
2345-5330
language English
publishDate 2024-09-01
publisher Pasteur Institute of Iran
record_format Article
series Journal of Medical Microbiology and Infectious Diseases
spelling doaj-art-4c251d6b70aa43ea9819dd4a55c9fefd2025-08-20T01:51:15ZengPasteur Institute of IranJournal of Medical Microbiology and Infectious Diseases2345-53492345-53302024-09-0112317117810.61186/JoMMID.12.3.171Variant Cells and Viral Infections: Understanding Cellular Coping MechanismsFarzaneh Sheikholeslami1*0https://orcid.org/0000-0003-2835-548XReza Shirzad11https://orcid.org/0000-0003-2122-9595Fatemeh Motevalli22https://orcid.org/0000-0003-4138-10841WHO Collaborating Center for Reference and Research on Rabies, Pasteur Institute of Iran, Tehran, Iran1WHO Collaborating Center for Reference and Research on Rabies, Pasteur Institute of Iran, Tehran, Iran2Department of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, IranCellular 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.https://jommid.pasteur.ac.ir/article-1-699-en.htmlviral infectionhostpathogen interactioncellular stress responseautophagyunfolded protein responseapoptosisendoplasmic reticulum stress stressviral replication
spellingShingle Farzaneh Sheikholeslami1*
Reza Shirzad1
Fatemeh Motevalli2
Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
Journal of Medical Microbiology and Infectious Diseases
viral infection
hostpathogen interaction
cellular stress response
autophagy
unfolded protein response
apoptosis
endoplasmic reticulum stress stress
viral replication
title Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
title_full Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
title_fullStr Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
title_full_unstemmed Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
title_short Variant Cells and Viral Infections: Understanding Cellular Coping Mechanisms
title_sort variant cells and viral infections understanding cellular coping mechanisms
topic viral infection
hostpathogen interaction
cellular stress response
autophagy
unfolded protein response
apoptosis
endoplasmic reticulum stress stress
viral replication
url https://jommid.pasteur.ac.ir/article-1-699-en.html
work_keys_str_mv AT farzanehsheikholeslami1 variantcellsandviralinfectionsunderstandingcellularcopingmechanisms
AT rezashirzad1 variantcellsandviralinfectionsunderstandingcellularcopingmechanisms
AT fatemehmotevalli2 variantcellsandviralinfectionsunderstandingcellularcopingmechanisms