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Related Experiment Video

Updated: Oct 5, 2025

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
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Endoplasmic Reticulum-Shaping Atlastin Proteins Facilitate KSHV Replication.

Wen-Ying Long1, Guo-Hua Zhao2, Yao Wu1

  • 1Central Laboratory, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Yiwu, China.

Frontiers in Cellular and Infection Microbiology
|January 31, 2022
PubMed
Summary

Atlastin proteins (ATLs) regulate Kaposi's sarcoma-associated herpesvirus (KSHV) infection by controlling its lytic activation. ATLs also impact cellular responses to endoplasmic reticulum (ER) stress, a known KSHV activator.

Keywords:
ER stressKSHVatlastinendoplasmic reticulumlytic activation

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Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Kaposi's sarcoma-associated herpesvirus (KSHV) exhibits latent and lytic life cycles.
  • The endoplasmic reticulum (ER) is crucial for KSHV production and ER stress can induce KSHV reactivation.
  • Factors regulating KSHV replication at the ER remain largely uncharacterized.

Purpose of the Study:

  • To investigate the role of Atlastin proteins (ATLs) in regulating KSHV lytic activation and infection.
  • To explore the connection between ATLs, ER stress, and KSHV replication.

Main Methods:

  • Overexpression and silencing of ATLs (ATL1, ATL2, ATL3) in cells.
  • Assessing KSHV lytic activation and infection levels.
  • Evaluating cellular response to ER stress.

Main Results:

  • Overexpression of ATLs enhanced KSHV lytic activation.
  • Silencing ATLs inhibited KSHV lytic activation and impaired cellular response to ER stress.
  • ER stress was observed to promote KSHV lytic activation.

Conclusions:

  • ATLs play a critical regulatory role in KSHV infection.
  • ATLs influence KSHV lytic activation through modulation of ER stress response.
  • This study expands the known functions of ATLs to include regulation of KSHV infection.