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Related Concept Videos

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 Extrinsic Apoptotic Pathway01:17

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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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A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...
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Viral genomes exhibit remarkable diversity in size, structure, and composition, influencing their replication strategies and interactions with host cells. These genomes consist of either DNA or RNA and may be linear or circular. Additionally, they can be single-stranded or double-stranded, with each configuration affecting how the virus propagates within a host. RNA viruses, for instance, generally have smaller genomes than DNA viruses, a factor that contributes to their high mutation rates and...
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Immune Response Against Viral Pathogens01:29

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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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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...
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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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Apoptosis in virus infection dynamics models.

Ruili Fan1, Yueping Dong, Gang Huang

  • 1a School of Mathematics and Physics , China University of Geosciences , Wuhan 430074 , China.

Journal of Biological Dynamics
|June 26, 2014
PubMed
Summary
This summary is machine-generated.

Increasing apoptosis can help control virus infections. However, in HIV patients, apoptosis

Keywords:
34K2092D30Hopf bifurcationapoptosisdiscrete delayvirus dynamics

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Area of Science:

  • Mathematical modeling
  • Virology
  • Immunology

Background:

  • Apoptosis, or programmed cell death, directly impacts uninfected cell populations.
  • Understanding apoptosis is crucial for modeling viral dynamics, particularly in HIV infections.

Purpose of the Study:

  • To extend existing virus infection models by incorporating activation-induced apoptosis.
  • To investigate the dual role of apoptosis in HIV infection dynamics, considering cytotoxic T lymphocyte immune response.
  • To analyze the impact of time-delayed apoptosis on infection stability.

Main Methods:

  • Development of two extended two-dimensional virus infection dynamics models.
  • Theoretical analysis of model stability with varying apoptosis rates.
  • Inclusion of cytotoxic T lymphocytes (CTLs) to represent immune response.
  • Incorporation of discrete-time delays in apoptosis.
  • Numerical simulations to validate theoretical findings.

Main Results:

  • Increased apoptosis generally aids in controlling viral infections.
  • In the context of HIV and CTL response, apoptosis can either promote or inhibit long-term infection evolution, depending on its intensity.
  • Time delays in apoptosis can lead to stability switching in the infection dynamics.
  • Numerical simulations confirm the theoretical predictions regarding apoptosis intensity and time delays.

Conclusions:

  • Apoptosis has a complex, context-dependent role in HIV infection dynamics.
  • The intensity and timing of apoptosis significantly influence the long-term outcome of HIV infection.
  • Mathematical modeling provides valuable insights into the intricate interplay between apoptosis, immune response, and viral persistence.