What is it about?

The novel coronavirus, also called “SARS-CoV-2” has infected millions of people globally, since 2020. While the virus mainly targets the lungs, it can also damage multiple other organs. But, exactly how it infects organs is unclear. The SARS-CoV-2 virus has a spike protein on its surface. This protein binds to an angiotensin converting enzyme 2 (ACE2) receptor on host cells, which helps the virus enter the cells. The cells of the immune system recognize these viruses through certain patterns that they identify as “foreign.” Then, they release inflammatory molecules to fight the infection. Host cells also have special proteins called “toll-like receptor” (TLR) proteins on their surface, which help in recognizing these patterns. New evidence suggests that the viral spike protein interacts strongly with one such receptor, known as TLR4. Based on these findings, the authors of this article proposed a possible mechanism by which SARS-CoV-2 infections occur. They suggest that the spike protein on the virus binds to TLR4 and activates it. This leads to an increase in ACE2 expression, which helps the virus to enter the cells. In the lungs, cells of the “alveoli” (specialized cup-like structures in the lungs) produce pulmonary surfactants, which normally block TLR4 and prevent infection. The SARS-CoV-2 virus destroys these cells, leading to an increase in the infection. In addition, the virus’s activation of TLR4 leads to abnormal TLR4 signaling, which leads to an increase in the inflammation in certain organs. This leads to multiple organ damage.

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Why is it important?

The model proposed by the authors highlights the major role of TLR4 in the development of the COVID-19 infection by SARS-CoV-2. Thus, targeting TLR4 through its antagonists might be a promising therapeutic option to treat patients with severe COVID-19. KEY TAKEAWAY: The SARS-CoV-2 virus may activate TLR4 receptors to enhance its entry into host cells. The inflammatory reactions caused by this activation lead to infection in multiple organs. Understanding this mechanism further can help identify possible targets for treatment of COVID-19.

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This page is a summary of: COVID-19 and Toll-Like Receptor 4 (TLR4): SARS-CoV-2 May Bind and Activate TLR4 to Increase ACE2 Expression, Facilitating Entry and Causing Hyperinflammation, Mediators of Inflammation, January 2021, Hindawi Publishing Corporation, DOI: 10.1155/2021/8874339.
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