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Updated: Aug 13, 2026

Measuring Endoplasmic Reticulum Stress and Unfolded Protein Response in HIV-1 Infected T-Cells and Analyzing its Role in HIV-1 Replication
10:12

Measuring Endoplasmic Reticulum Stress and Unfolded Protein Response in HIV-1 Infected T-Cells and Analyzing its Role in HIV-1 Replication

Published on: June 14, 2024

Viruses, endoplasmic reticulum stress, and interferon responses

B He1

  • 1Department of Microbiology and Immunology, College of Medicine, The University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, IL 60612, USA. tshuo@uic.edu

Cell Death and Differentiation
|January 7, 2006
PubMed

Insights

Viruses trigger cellular stress responses like endoplasmic reticulum (ER) stress and interferon production. To replicate, viruses must overcome these defenses, including the double-stranded RNA-dependent protein kinase (PKR).

Area of Science:

  • Virology
  • Immunology
  • Cellular Biology

Background:

  • Viral infections induce both interferon responses and endoplasmic reticulum (ER) stress.
  • Interferon responses are triggered by viral double-stranded RNA, while ER stress is induced by viral proteins.
  • The double-stranded RNA-dependent protein kinase (PKR) is a key interferon-regulated protein that limits viral replication.

Purpose of the Study:

  • To review recent advances in understanding how viruses interact with ER stress and interferon responses.
  • To explore viral strategies for overcoming cellular defense mechanisms.
  • To highlight the complex interplay between viral replication and host cell stress pathways.

Main Methods:

  • This review synthesizes findings from recent scientific literature.
  • It focuses on the molecular mechanisms by which viruses manipulate host cell responses.
  • Key areas examined include PKR function and ER stress-induced pathways.

Main Results:

  • Viruses have evolved mechanisms to counteract the antiviral effects of PKR.
  • ER stress, while potentially leading to apoptosis, is also manipulated by viruses.
  • Viruses interfere with interferon signaling and exploit ER stress pathways to facilitate replication and pathogenesis.

Conclusions:

  • Viruses actively manipulate both interferon responses and ER stress pathways.
  • Understanding these viral strategies is crucial for developing antiviral therapies.
  • The complex interplay between viruses and host cell stress offers insights into viral pathogenesis.

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