Coronaviruses and Integrin αvβ3: Does Thyroid Hormone Modify the Relationship?

Area of Science:

• Cell biology
• Virology
• Endocrinology

Background:

• Coronavirus entry into target cells involves binding to cell ectoenzymes, with angiotensin-converting enzyme-2 (ACE2) identified for SARS-CoV-2.
• Plasma membrane integrins, such as integrin αvβ3, are implicated in the internalization and replication of coronaviruses.
• ACE2 activity is modulated by intracellular signaling generated by integrins.

Purpose of the Study:

• To investigate the role of integrin αvβ3 internalization in coronavirus uptake.
• To evaluate the potential contribution of clinical host L-thyroxine (T4) to coronavirus target cell uptake and its consequences.

Main Methods:

• The study proposes that integrin αvβ3 internalization is a mechanism for coronavirus uptake.
• It evaluates the influence of L-thyroxine (T4) on this process.

Main Results:

• The viral binding domain on integrin αvβ3 is located near the Arg-Gly-Asp (RGD) peptide-binding site, suggesting RGD molecules can impact virus binding.
• L-thyroxine (T4) binds to integrin αvβ3, modulating its affinity for other proteins, controlling its internalization, and regulating cytokine gene expression.

Conclusions:

• L-thyroxine (T4) may influence coronavirus uptake by target cells through integrin αvβ3.
• Thyroid hormone analogues, including deaminated T4 and deaminated 3,5,3'-triiodo-L-thyronine (T3), are potential agents to block T4's virus-relevant actions at integrin αvβ3, potentially restricting viral uptake.