SARS-CoV-2 Suppresses Membrane Complement Regulatory Proteins, Making Blood Vessels More Vulnerable to Damage.
Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 02, 2025 18 hours, 43 minutes ago
Medical News:
Scientists uncover how SARS-CoV-2 damages blood vessels
A team of researchers from Zhejiang University School of Medicine, Naval Medical University, Tongji Medical College, Nankai University, and the Chinese Academy of Medical Sciences has made a groundbreaking discovery about how SARS-CoV-2, the virus responsible for COVID-19, damages blood vessels. Their study reveals that the virus suppresses the body's natural defense system against blood vessel damage, leading to severe complications.
COVID-19 is known to cause serious damage to blood vessels, a condition called endothelial injury, which can result in severe inflammation and blood clots. However, until now, scientists did not fully understand how the virus weakens these blood vessels. This
Medical News report explains how SARS-CoV-2 interferes with the body's defense mechanisms, making blood vessels more vulnerable to damage.
How SARS-CoV-2 weakens blood vessel protection
The researchers discovered that SARS-CoV-2 produces specific proteins - M, NSP16, and ORF9b - that interfere with the body's complement regulatory proteins (CRPs). CRPs act as a shield, preventing the immune system from attacking the body's own blood vessels. However, when these SARS-CoV-2 proteins are present, they weaken this protective shield, making blood vessels more vulnerable to attack by the immune system.
In healthy individuals, CRPs such as CD55 and CD59 protect blood vessels by preventing excessive activation of the complement system - a part of the immune system that helps clear infections but can also cause tissue damage if not properly controlled. The study found that the SARS-CoV-2 proteins block the function of these protective CRPs, allowing the complement system to attack and damage blood vessels, leading to severe complications such as blood clot formation and inflammation.
Key study findings
The study identified three key regulators of CRPs in blood vessels: ADAMTS9, SYAP1, and HIGD1A. These molecules play a crucial role in maintaining the protective function of CD55 and CD59. However, the SARS-CoV-2 proteins M, NSP16, and ORF9b inhibit these regulators, reducing the protective ability of CRPs.
Interestingly, the researchers also found that certain immune signaling proteins, known as interferons (IFNs), can help restore CRP protection. IFN-γ (gamma interferon), in particular, was able to counteract the harmful effects of SARS-CoV-2 proteins and restore CD55 and CD59 function. This finding suggests that interferon-based therapies could potentially help protect blood vessels in severe COVID-19 cases.
Additionally, the researchers observed that severe COVID-19 patients had increased deposits of complement system components such as FCN1 and C5b-9 in their blood vessels. These deposits indicate that the complement system is being excessively activated, leading to widespread endothelial damage and contributing to the severe complications seen in critical COVID-19 patients.
Potential treatment approaches
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Based on their findings, the researchers suggest that therapies aimed at preserving CRP function or controlling complement system activation could help prevent severe COVID-19 complications. Drugs that selectively block the formation of the membrane attack complex (MAC), which is formed by the complement system, may offer a promising treatment approach.
Some existing drugs, such as eculizumab and ravulizumab, which target specific components of the complement system, have already shown benefits in small groups of COVID-19 patients. However, these treatments carry potential risks, including increased susceptibility to bacterial infections. Therefore, more research is needed to develop targeted therapies that specifically protect blood vessels without compromising the immune system’s ability to fight infections.
Conclusion
This study sheds new light on how SARS-CoV-2 disrupts the body's natural defenses and causes severe damage to blood vessels. By blocking the protective functions of CRPs, the virus makes blood vessels more vulnerable to attack by the immune system. The discovery of interferon’s role in counteracting this effect provides hope for potential new treatments that could reduce severe complications in COVID-19 patients.
The findings also highlight the importance of targeting the complement system in severe COVID-19 cases. Therapies that restore CRP function or selectively block complement activation could help prevent life-threatening complications such as blood clots and organ failure. As scientists continue to explore these treatment options, their work brings us closer to understanding and controlling the devastating effects of COVID-19.
The study findings were published in the peer-reviewed journal: Emerging Microbes & Infections.
https://www.tandfonline.com/doi/full/10.1080/22221751.2025.2467781
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