Related Experiment Video

Updated: Mar 27, 2026

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
06:02

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors

Published on: September 13, 2018

7.5K

Apoptosis, autophagy and unfolded protein response pathways in Arbovirus replication and pathogenesis

Mahmoud Iranpour1, Adel Rezaei Moghadam2, Mina Yazdi3

  • 1Zoonotic Diseases and Special Pathogens,National Microbiology Laboratory,Public Health Agency of Canada,1015 Arlington St.,Winnipeg,Manitoba,Canada.

Expert Reviews in Molecular Medicine
|January 20, 2016
PubMed

Insights

Arboviruses pose global health risks. This review explores how apoptosis, autophagy, and the unfolded protein response (UPR) impact arbovirus infection and replication, offering insights into disease pathogenesis.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Arboviruses are significant global pathogens, with vaccines available for some but treatment and prevention remaining challenges.
  • Viral replication involves complex regulatory mechanisms, including cellular processes like apoptosis, autophagy, and the unfolded protein response (UPR).

Purpose of the Study:

  • To review the critical roles of apoptosis, autophagy, and UPR in arbovirus replication and infection.
  • To elucidate the regulatory functions of these cellular pathways in arbovirus pathogenesis.

Main Methods:

  • Literature review focusing on apoptosis, autophagy, and UPR.
  • Analysis of existing research on arbovirus-host interactions.
  • Synthesis of information on the initiation and regulation of apoptosis, autophagy, and UPR.

Main Results:

  • Apoptosis, autophagy, and UPR are integral to the life cycle of many viruses, including arboviruses.
  • These pathways can be manipulated by arboviruses to facilitate replication or by the host to restrict it.
  • Understanding these host-pathogen interactions is key to developing novel therapeutic strategies.

Conclusions:

  • Apoptosis, autophagy, and UPR are crucial cellular mechanisms influencing arbovirus pathogenesis.
  • Targeting these pathways presents a potential avenue for future arbovirus disease control strategies.
  • Further research into the intricate interplay between arboviruses and these cellular responses is warranted.

More Related Videos

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection08:16

Identifying Caspases and their Motifs that Cleave Proteins During Influenza A Virus Infection

Published on: July 21, 2022

1.9K
Establishment of Viral Infection and Analysis of Host-Virus Interaction in Drosophila Melanogaster09:57

Establishment of Viral Infection and Analysis of Host-Virus Interaction in Drosophila Melanogaster

Published on: March 14, 2019

11.4K

Related Concept Videos

Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
19
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
5.0K
The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
6.8K
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
17
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.3K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.2K