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Related Experiment Video

Updated: May 29, 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

Molecules from apoptotic pathways modulate HIV-1 replication in Jurkat cells.

Xue Wang¹, Viswanath Ragupathy, Jiangqin Zhao

¹Laboratory of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA. xue.wang@fda.hhs.gov

Biochemical and Biophysical Research Communications

|September 28, 2011

Summary

Human immunodeficiency virus type 1 (HIV-1) replication is enhanced by pro-apoptotic proteins and inhibited by anti-apoptotic molecules. Targeting apoptosis may offer new strategies for inhibiting HIV-1 infection.

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Evaluation of the Efficacy And Toxicity of RNAs Targeting HIV-1 Production for Use in Gene or Drug Therapy

Evaluation of the Efficacy And Toxicity of RNAs Targeting HIV-1 Production for Use in Gene or Drug Therapy

Published on: September 5, 2016

Area of Science:

Virology
Cell Biology
Immunology

Background:

Viral replication intricately modulates host cell processes, including metabolism and apoptosis.
The precise role of apoptosis-associated molecules in human immunodeficiency virus type 1 (HIV-1) replication and viral yield remains incompletely understood.

Purpose of the Study:

To investigate the relationship between apoptosis-associated molecules and HIV-1 production.
To determine if modulating apoptotic pathways impacts HIV-1 replication.

Main Methods:

Utilized the Jurkat cell line, a susceptible model for HIV-1 infection.
Employed sensitive real-time RT-PCR assays to quantify viral production.
Investigated the effects of pro- and anti-apoptotic molecules, gene knockdown (siRNA, antisense mRNA), and caspase-3 inhibition on HIV-1 replication.

Main Results:

Increased expression of pro-apoptotic proteins (FasL, FADD, p53) significantly enhanced HIV-1 production.
Decreased expression of anti-apoptotic molecules (FLIP, Bcl-X(L), XIAP) reduced HIV-1 production.
Knockdown of Bax and FADD, along with caspase-3 inhibition, suppressed viral replication and production.

Conclusions:

HIV-1 infection actively manipulates the host cell's apoptotic machinery to promote viral replication.
Inhibiting apoptosis presents a potential therapeutic strategy to impede HIV-1 replication and mitigate its cytopathic effects.
MAPK signaling pathways and apoptosis are key factors influencing HIV-1 replication.