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Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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...
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Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Apoptosis01:30

Apoptosis

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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...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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...
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Leaky Scanning02:28

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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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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. 
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Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
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Regulation of Apoptosis by Enteroviruses.

Yalan Lai1,2,3, Mingshu Wang1,2,3, Anchun Cheng1,2,3

  • 1Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

Frontiers in Microbiology
|June 26, 2020
PubMed
Summary

Enteroviruses manipulate host cell apoptosis, initially inhibiting it for replication, then inducing it later to spread. This balance is key to viral survival and disease.

Keywords:
apoptotic pathwaybalanceenterovirusregulationviral replication

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Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Enterovirus infections pose significant health risks to various organisms.
  • Host defense mechanisms, including apoptosis, combat viral infections.
  • Enteroviruses have evolved complex strategies to evade or manipulate apoptosis for their own benefit.

Purpose of the Study:

  • To elucidate the intricate mechanisms by which enteroviruses regulate host cell apoptosis.
  • To understand the temporal dynamics of apoptosis manipulation by enteroviruses during infection.
  • To identify viral strategies that create a favorable environment for enterovirus replication and proliferation.

Main Methods:

  • Review and synthesis of existing literature on enterovirus-host interactions.
  • Analysis of molecular pathways involved in apoptosis regulation (e.g., PI3K/Akt, autophagy).
  • Examination of viral protein functions in modulating host cell processes.

Main Results:

  • Enteroviruses initially suppress apoptosis via pathways like PI3K/Akt and autophagy to promote early replication.
  • In later infection stages, enteroviruses induce apoptosis using viral proteins to facilitate spread.
  • A temporal balance or competition between apoptosis inhibition and induction is crucial for enterovirus survival.

Conclusions:

  • Enteroviruses exhibit a sophisticated, stage-specific regulation of apoptosis.
  • Understanding these mechanisms is vital for developing antiviral strategies against enteroviruses and related picornaviruses.
  • The interplay between viral replication and host apoptosis is a critical determinant of disease severity.