Related Experiment Video

Updated: May 21, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Viral subversion of autophagy impairs oncogene-induced senescence

Andrew M Leidal1, Patrick W K Lee, Craig McCormick

  • 1Department of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.

Autophagy
|June 28, 2012
PubMed

Insights

Kaposi's sarcoma-associated herpesvirus (KSHV) hijacks cellular autophagy to promote cancer development by enabling infected cells to bypass senescence. This viral strategy aids KSHV persistence and proliferation.

Area of Science:

  • Virology
  • Cellular Biology
  • Oncology

Background:

  • Viruses often manipulate host cell processes like autophagy for their benefit.
  • Kaposi's sarcoma-associated herpesvirus (KSHV) causes persistent infections and is linked to cancers.
  • KSHV's interaction with autophagy and its role in disease are not fully understood.

Purpose of the Study:

  • To investigate how KSHV utilizes the autophagy pathway.
  • To determine the role of KSHV-modulated autophagy in viral pathogenesis and cancer development.

Main Methods:

  • The study likely involved cell culture experiments using KSHV-infected cells.
  • Techniques to monitor autophagy and oncogene-induced senescence (OIS) were probably employed.
  • Analysis of KSHV gene products' effects on cellular processes was central.

Main Results:

  • KSHV actively subverts the host cell's autophagy machinery.
  • This viral subversion allows infected cells to bypass oncogene-induced senescence (OIS), a tumor-suppressing mechanism.
  • KSHV's manipulation of autophagy facilitates viral persistence and cell proliferation.

Conclusions:

  • KSHV exploits autophagy to create a favorable environment for infection.
  • By inhibiting senescence, KSHV promotes tumor initiation and progression.
  • Targeting KSHV's autophagy manipulation could be a therapeutic strategy.
Keywords:
DNA damageKSHVautophagyoncogeneoncogene-induced senescence

More Related Videos

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry11:39

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Published on: July 21, 2017

Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy09:59

Quantitative Analysis of Autophagy using Advanced 3D Fluorescence Microscopy

Published on: May 3, 2013

Related Concept Videos

Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Autophagic Cell Death01:18

Autophagic Cell Death

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 pro-apoptotic...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...