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

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

9.4K
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...
9.4K
Apoptosis01:30

Apoptosis

17.1K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
17.1K
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

5.7K
Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized...
5.7K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

9.3K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.3K
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

2.6K
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...
2.6K
Autophagic Cell Death01:18

Autophagic Cell Death

5.1K
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...
5.1K

You might also read

Related Articles

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

Sort by
Same author

Oropouche virus infects human neural progenitor cells and alters the growth of brain organoids.

iScience·2026
Same author

BK Polyomavirus Genetic Diversity and Evolution in Kidney Transplant Recipients with Viral Nephropathy Using Whole Genome Sequencing.

The Journal of infectious diseases·2026
Same author

Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants.

iScience·2025
Same author

Structural basis of poxvirus fusion regulation and anti-A16/G9 antibody-mediated neutralization and protection.

Cell·2025
Same author

Distribution and disturbances of ditches across salt marshes of the Northeast U.S. with implications for management and restoration.

Journal of environmental management·2025
Same author

Structural insights into tecovirimat antiviral activity and poxvirus resistance.

Nature microbiology·2025
Same journal

Reframing risk assessment for malaria elimination in a changing climate.

Nature reviews. Microbiology·2026
Same journal

Bacterial vesicles protect the membrane during polymyxin stress.

Nature reviews. Microbiology·2026
Same journal

Fermented food microbiome: influence on oral and gut microbiota, and human health.

Nature reviews. Microbiology·2026
Same journal

Klebsiella genus as driver of human disease: from infections to non-communicable disorders.

Nature reviews. Microbiology·2026
Same journal

Coupling experiments and macroecological models to resolve multi-stressor effects in vector-pathogen systems.

Nature reviews. Microbiology·2026
Same journal

A new antibiotic scaffold hits a new target.

Nature reviews. Microbiology·2026
See all related articles

Related Experiment Video

Updated: Apr 11, 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

3.0K

Viral apoptotic mimicry.

Ali Amara1, Jason Mercer2

  • 1Institut National de la Santé et de la Recherche Médicale U944 and Centre National de la Recherche Scientifique UMR 7212, Laboratoire de Pathologie et Virologie Moléculaire, Institut Universitaire d'Hématologie, Université Paris Diderot, Sorbonne Paris Cité, Hôpital Saint-Louis, 1 avenue Claude Vellefaux, 75010 Paris, France.

Nature Reviews. Microbiology
|June 9, 2015
PubMed
Summary
This summary is machine-generated.

Viruses use "apoptotic mimicry," exposing a host cell signal on their surface, to infect cells and evade the immune system. This strategy is common in enveloped viruses and is being explored for therapeutic targets.

More Related Videos

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy
08:51

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy

Published on: April 3, 2018

9.6K
Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
13:54

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

11.4K

Related Experiment Videos

Last Updated: Apr 11, 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

3.0K
Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy
08:51

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy

Published on: April 3, 2018

9.6K
Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
13:54

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

11.4K

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Viruses are opportunistic pathogens that employ sophisticated strategies to infect host cells.
  • Viral apoptotic mimicry, characterized by the display of phosphatidylserine on the viral surface, is a key mechanism for viral entry and replication.
  • This strategy is increasingly recognized as a common theme among various viruses.

Purpose of the Study:

  • To summarize the current understanding of viral apoptotic mimicry as a mechanism for virus entry, binding, and immune evasion.
  • To highlight key examples of enveloped viruses utilizing this strategy.
  • To explore emerging examples in non-enveloped viruses and discuss future therapeutic applications.

Main Methods:

  • Review of existing literature on viral apoptotic mimicry.
  • Focus on four well-described examples: vaccinia virus, dengue virus, Ebola virus, and pseudotyped lentivirus.
  • Analysis of mechanisms for virus entry, binding, and immune evasion related to apoptotic mimicry.

Main Results:

  • Apoptotic mimicry is a prevalent strategy employed by enveloped viruses for infection.
  • Phosphatidylserine exposure on the viral surface facilitates host cell manipulation.
  • Recent evidence suggests non-enveloped viruses also utilize this mimicry strategy.

Conclusions:

  • Viral apoptotic mimicry is a critical mechanism for viral pathogenesis and immune evasion.
  • Understanding this process offers potential avenues for therapeutic intervention.
  • Further research into viral mimicry strategies is warranted to develop novel antiviral therapies.