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Related Concept Videos

Autophagy01:27

Autophagy

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Delivery Pathways to the Lysosome01:36

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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
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Autophagic Cell Death01:18

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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.
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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Receptor-mediated Endocytosis01:20

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Intracellular Movement of Viruses and Bacteria01:10

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Intracellular bacteria and viruses often comprise a group of highly infectious pathogens that can cause several diseases. Bacterial pathogens include those belonging to the genus Rickettsia responsible for conditions such as rocky mountain spotted fever and the Mediterranean spotted fever; Chlamydia, a genus responsible for a sexually transmitted disease; Coxiella burnetii, an agent responsible for Q fever. Viral pathogens include vaccinia—a poxvirus, and herpes simplex virus—a...
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Related Experiment Video

Updated: Feb 26, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
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The Interaction between Nidovirales and Autophagy Components.

Yingying Cong1, Pauline Verlhac2, Fulvio Reggiori3

  • 1Department of Cell Biology, University of Groningen, University Medical Center Groningen, A. Deusinglaan 1, 9713 AV Groningen, The Netherlands. y.cong@umcg.nl.

Viruses
|July 12, 2017
PubMed
Summary

Viruses in the Nidovirales order hijack cellular autophagy for replication. This review explores the mechanisms and implications of this viral strategy, highlighting its importance in pathogenesis.

Keywords:
arterivirusautophagic fluxautophagosomecoronavirusegressioninfectionmesonivirusreplicationronivirus

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Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Autophagy is a cellular process for degrading damaged components, crucial for maintaining homeostasis.
  • Many viruses exploit the autophagy pathway to aid their replication and survival within host cells.
  • Nidovirales, a group of RNA viruses including coronaviruses, are known to induce cellular membrane rearrangements.

Purpose of the Study:

  • To review the current understanding of the interaction between Nidovirales and the autophagy pathway.
  • To elucidate the potential mechanisms by which Nidovirales usurp autophagy.
  • To highlight the significance of this interplay in viral pathogenesis.

Main Methods:

  • Literature review of existing studies on autophagy and Nidovirales.
  • Analysis of viral-host interactions at the molecular level.
  • Synthesis of current knowledge on autophagy induction by Nidovirales.

Main Results:

  • Nidovirales induce significant membrane rearrangements, including autophagosome formation, in host cells.
  • Evidence suggests that Nidovirales actively manipulate the autophagy machinery for their benefit.
  • The precise mechanisms and full extent of autophagy usurpation by Nidovirales are still under investigation.

Conclusions:

  • Nidovirales likely utilize autophagy to facilitate their replication and spread.
  • Further research is needed to fully understand the complex interplay between Nidovirales and host autophagy.
  • Targeting this interaction could offer novel therapeutic strategies against Nidovirales infections.