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12:02
Assays for the Identification of Novel Antivirals against Bluetongue Virus
Published on: October 11, 2013
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Decoding the enigma of antiviral crisis: Does one target molecule regulate all?
Abdullah Mahmud-Al-Rafat1, Apurba Majumder2, K M Taufiqur Rahman3
1Research & Development Division, Incepta Vaccine Ltd., Zirabo, Savar, Dhaka 1341, Bangladesh; Biotechnology and Genetic Engineering Discipline, Khulna University, Khulna 9208, Bangladesh.
Cytokine
|January 8, 2019
Summary
Excessive inflammation, or cytokine storms, contribute to fatal viral infections like Ebola and SARS-CoV. Targeting Interleukin-6 (IL-6) signaling via ADAM-17 may offer novel antiviral strategies to control these responses.
Area of Science:
- Immunology
- Virology
- Drug Discovery
Background:
- Cytokine storms, driven by excessive pro-inflammatory responses, are linked to fatalities in viral infections such as Ebola, SARS-CoV, and dengue.
- Interleukin-6 (IL-6) plays a dual role, mediating pro-inflammatory responses via trans-signaling and anti-inflammatory responses via classical-signaling.
Purpose of the Study:
- To explore IL-6 signaling pathways as a target for novel antiviral agents.
- To identify molecular mechanisms regulating the switch between IL-6 trans- and classical-signaling.
Main Methods:
- Review of existing literature on cytokine storms, IL-6 signaling, and antiviral therapies.
- Analysis of the role of the tumor necrosis factor-α converting enzyme (ADAM-17) in regulating IL-6 receptor interactions.
Main Results:
- IL-6's pro-inflammatory effects are mediated by its soluble receptor (sIL-6R) and trans-signaling.
- Anti-inflammatory effects are mediated by the membrane-bound IL-6 receptor (IL-6R) and classical-signaling.
- ADAM-17 is proposed as a key regulator of the switch between IL-6 signaling pathways.
Conclusions:
- Targeting the IL-6 signaling switch mechanism presents a promising strategy for developing broad-spectrum antiviral drugs.
- ADAM-17 is identified as a potential master molecule for regulating host responses to viral infections.
- Modulating ADAM-17 activity could limit severe inflammatory responses and prevent fatal outcomes from viral diseases.
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