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Updated: May 30, 2026

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

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Published on: June 14, 2024

Endoplasmic reticulum stress causes EBV lytic replication.

Gwen Marie Taylor¹, Sandeep K Raghuwanshi, David T Rowe

¹Department of Pathology, University of Pittsburgh and Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.

|August 19, 2011

Summary

This summary is machine-generated.

Endoplasmic reticulum (ER) stress activates Epstein-Barr virus (EBV) lytic replication in lymphoblastoid cell lines (LCLs). Salubrinal (SAL) enhances this effect and also exhibits independent antiviral properties, impacting virus release and gp350 expression.

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Area of Science:

Cellular biology
Virology
Immunology

Background:

Endoplasmic reticulum (ER) stress is a cellular response to misfolded proteins.
Epstein-Barr virus (EBV) can establish latency or undergo lytic replication in B cells.

Purpose of the Study:

To investigate the role of ER stress in EBV lytic replication.
To explore the effects of thapsigargin (TG) and Salubrinal (SAL) on EBV reactivation.

Main Methods:

Treatment of lymphoblastoid cell lines (LCLs) with ER stress inducers (TG, SAL).
Analysis of EBV gene expression (immediate-early, early, late genes) and gp350 surface expression.
Assessment of virus release and B-cell phenotype markers (BCL6, BLIMP1, CD138).
Microarray analysis to identify candidate genes involved in lytic replication.

Main Results:

Thapsigargin (TG) alone induced EBV lytic gene activation, gp350 expression, and virus release in LCLs.
Salubrinal (SAL) synergized with TG to enhance EBV lytic gene induction.
SAL demonstrated both ER-stress-dependent and -independent antiviral effects, inhibiting virus release and gp350 expression.
TG treatment maintained a germinal center B-cell phenotype (BCL6 expression).

Conclusions:

ER stress is a potent trigger for EBV lytic replication.
SAL possesses dual antiviral activities, modulating EBV replication and release.
ER stress influences B-cell phenotype during EBV infection.