Related Experiment Video
Updated: Nov 14, 2025

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts
Published on: October 9, 2016
Contribution of STAT3 to the pathogenesis of COVID-19
Abdollah Jafarzadeh1, Maryam Nemati2, Sara Jafarzadeh3
1Department of Immunology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran; Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Insights
Signal transducer and activator of transcription-3 (STAT-3) contributes to severe COVID-19 by promoting inflammation and suppressing antiviral immunity. Targeting STAT-3 may offer a novel therapeutic strategy for treating this viral disease.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- COVID-19 pathogenesis involves hyper-inflammation, cytokine storms, and immune dysregulation.
- Signal transducer and activator of transcription-3 (STAT-3) is a key intracellular signaling molecule implicated in immune responses.
Purpose of the Study:
- To elucidate the role of STAT-3 in COVID-19 pathogenesis.
- To explore STAT-3 as a potential therapeutic target for COVID-19 treatment.
Main Methods:
- Review and analysis of existing literature on STAT-3 signaling in viral infections and inflammation.
- Discussion of STAT-3's molecular mechanisms in the context of SARS-CoV-2 infection.
Main Results:
- STAT-3 activation exacerbates inflammatory responses and cytokine storms in severe COVID-19.
- STAT-3 suppresses crucial antiviral interferon responses.
- STAT-3 influences adaptive immunity, promoting Th17 responses and impairing Th1/Treg balance.
- STAT-3 contributes to M2 macrophage polarization, lung fibrosis, and thrombosis.
Conclusions:
- STAT-3 plays a multifaceted role in promoting COVID-19 pathogenesis.
- Targeting STAT-3 presents a promising therapeutic avenue for managing severe COVID-19 and its complications.
Abstract:
Hyper-inflammatory responses, lymphopenia, unbalanced immune responses, cytokine storm, large viral replication and massive cell death play fundamental roles in the pathogenesis of COVID-19. Extreme production of many kinds of pro-inflammatory cytokines and chemokines occur in severe COVID-19 that called cytokine storm. Signal transducer and activator of transcription-3 (STAT-3) present in the cytoplasm in an inactive form and can be stimulated by a vast range of cytokines, chemokines and growth factors. Thus, STAT-3 can participate in the induction of inflammatory responses during coronavirus infections. STAT-3 can also suppress anti-virus interferon response and induce unbalanced anti-virus adaptive immune response, through influencing Th17-, Th1-, Treg-, and B cell-mediated functions. Furthermore, STAT-3 can contribute to the M2 macrophage polarization, lung fibrosis and thrombosis. Moreover, STAT-3 may be directly targeted by some virus-derived protein and operate as a pro-viral or anti-viral element in a virus-specific process. Here, the possible contribution of STAT-3 to the pathogenesis of COVID-19 was explained, while providing potential approaches to target this transcription factor in an attempt for COVID-19 treatment.
Related Concept Videos
The JAK-STAT Signaling Pathway
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
PI3K/mTOR/AKT Signaling Pathway
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
TGF - β Signaling Pathway

