CD147 and Cyclophilin Enables SARS-CoV-2 Infection of Human Monocytes and Activation of Toll-Like-Receptors
Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 03, 2025 1 month, 2 days, 19 hours, 54 minutes ago
Medical News: Understanding How SARS-CoV-2 Infects Monocytes
A new study conducted by researchers from the Medical University of Vienna, Austria, has unveiled a critical pathway that enables SARS-CoV-2 to infect human monocytes. This groundbreaking research provides new insights into how the virus evades immune responses and contributes to inflammation in COVID-19 patients. This
Medical News report delves into the findings of this study and its potential implications for therapeutic interventions.
CD147 and Cyclophilin Enables SARS-CoV-2 Infection of Human Monocytes and Activation
of Toll-Like-Receptors
Monocytes, a type of white blood cell, play a crucial role in the body's defense against infections. They serve as a first line of immune defense, recognizing pathogens and triggering immune responses. However, their uncontrolled activation can lead to excessive inflammation, a hallmark of severe COVID-19 cases. The study found that SARS-CoV-2 exploits a specific cellular interaction between Cyclophilin and CD147 to infect monocytes and subsequently activate Toll-like receptors (TLRs) 7 and 8, which are key components of the immune system's response to viral infections.
The Key Findings of the Study
-SARS-CoV-2 Uses an Alternative Entry Mechanism
One of the most significant revelations of the study is that SARS-CoV-2 does not rely on the well-known ACE2 receptor to infect monocytes. Instead, the virus uses CD147, a receptor commonly expressed on monocytes, as an alternative pathway. CD147 binds to Cyclophilins A and B, which are incorporated into the virus particles, allowing SARS-CoV-2 to enter monocytes.
This discovery challenges previous assumptions that ACE2 was the only gateway for SARS-CoV-2 entry into human cells.
-Activation of Toll-Like Receptors 7 and 8
After entering the monocytes, SARS-CoV-2 triggers a strong immune response by activating TLR7 and TLR8. These receptors are designed to recognize viral RNA and mount an immune defense. However, their activation by SARS-CoV-2 leads to an overproduction of inflammatory molecules, including tumor necrosis factor (TNF), interleukin-1 beta (IL-1b), and interleukin-6 (IL-6), which contribute to the hyperinflammation seen in severe COVID-19 cases.
-CD147 Blocking Reduces SARS-CoV-2 Infection
To further confirm the role of CD147 in SARS-CoV-2 infection, researchers tested the effects of blocking CD147 with specific antibodies. They found that this approach significantly reduced viral entry into monocytes, suggesting that targeting CD147 could be a potential strategy to prevent monocyte infection and mitigate severe inflammation.
Implications for COVID-19 Treatment
These findings open up new possibilities for therapeutic interventions aimed at reducing severe COVID-19 inflammation. If CD147 plays a crucial role in viral entry and immune activation, blocking this path
way could help prevent the excessive immune response that contributes to severe disease outcomes. This approach could be particularly useful for high-risk patients who are more susceptible to severe COVID-19 complications.
Conclusion
This study highlights a novel mechanism through which SARS-CoV-2 infects human monocytes using CD147 and Cyclophilins, bypassing the traditional ACE2 receptor. The activation of TLR7 and TLR8 following viral entry results in a pro-inflammatory response that contributes to severe COVID-19 symptoms. By targeting CD147, researchers may be able to develop new treatment strategies to reduce inflammation and improve patient outcomes. These findings not only enhance our understanding of SARS-CoV-2 infection but also pave the way for potential therapeutic advancements in the fight against COVID-19.
The study findings were published in the peer-reviewed journal: Frontiers in Immunology.
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1460089/full
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