Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A Novel Workflow to Estimate Limb Orientation from Wearable Sensors to Monitor Infant Motor Development.

Sensors (Basel, Switzerland)·2026
Same author

vIRA Inhibition of Antiviral Necroptosis and RIPK3 Binding Are Separable Events.

Pathogens (Basel, Switzerland)·2026
Same author

Characterizing the interactions between murine cytomegalovirus M72 and the carbon catabolite repression 4-negative on TATA-less (CCR4-NOT) complex.

Virology·2026
Same author

Host cell Z-RNAs activate ZBP1 during virus infections.

Nature·2025
Same author

RIPK1 is required for ZBP1-driven necroptosis in human cells.

PLoS biology·2025
Same author

Perspective on the 65-Year Anniversary of the Discovery of Cytomegalovirus.

Viruses·2025

Related Experiment Video

Updated: May 10, 2026

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
09:15

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

Viral modulation of programmed necrosis.

William J Kaiser1, Jason W Upton, Edward S Mocarski

  • 1Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA 30322, USA.

Current Opinion in Virology
|June 19, 2013
PubMed
Summary

Viruses and host defenses engage in an evolutionary arms race, with caspase 8 acting as a central regulator of apoptosis and programmed necrosis. This balance shapes host-pathogen interactions.

More Related Videos

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Related Experiment Videos

Last Updated: May 10, 2026

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
09:15

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Area of Science:

  • Cellular biology
  • Immunology
  • Virology

Background:

  • Apoptosis and programmed necrosis are key host defense mechanisms against viral infections.
  • Viruses have evolved countermeasures, including B cell leukemia (BCL)2-like suppressors, to evade intrinsic apoptosis.
  • Extrinsic apoptosis and programmed necrosis evolved as subsequent defense strategies.

Purpose of the Study:

  • To elucidate the evolutionary interplay between host cell death pathways and viral countermeasures.
  • To understand the role of caspase 8 as a central regulator in this dialog.

Main Methods:

  • Comparative analysis of apoptosis and programmed necrosis pathways.
  • Examination of viral strategies to inhibit host cell death.
  • Investigating the activation triggers of receptor interacting protein (RIP)3 kinase (RIPK3).

Main Results:

  • Intrinsic apoptosis is modulated by viral BCL2-like suppressors.
  • Extrinsic apoptosis, regulated by caspase 8, emerged to bypass intrinsic apoptosis suppressors.
  • Programmed necrosis, involving RIPK3, acts as a backup to extrinsic apoptosis when caspase 8 or RIP1 is inhibited.
  • Caspase 8 functions as a critical 'supersensor' controlling both cell death pathways.

Conclusions:

  • The evolution of cell death pathways is driven by viral pressures.
  • Caspase 8 plays a pivotal role in orchestrating apoptosis and programmed necrosis.
  • Understanding this balance is crucial for developing antiviral strategies.