Mice Study Identifies Fibrin as the Key Driver of Long COVID

 
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A recent study has revolutionized the understanding of long COVID by identifying fibrin, a blood clotting protein, as the main culprit behind the persistent symptoms. The study challenges the current belief that inflammation triggered by the virus is responsible for long COVID, instead revealing that fibrin accumulation due to SARS-CoV-2’s spike protein leads to clotting and vascular damage, which underpins the majority of complications.

The Study and Its Revelations

Published on August 28, 2024, this research used a mouse model of COVID-19 to investigate why millions suffer from long COVID symptoms such as neurological issues, heart complications, and stroke-like effects. The study highlights that the spike protein itself is responsible for fibrin buildup, which in turn clogs the blood vessels and triggers inflammation. While initial COVID-19 infection symptoms tend to subside, fibrin continues to accumulate in the bloodstream, leading to post-acute sequelae, or long COVID, in many cases.

This finding overturns the previous model of long COVID, which attributed the condition primarily to inflammatory damage caused by the virus. Instead, it suggests that fibrin, rather than the virus itself, is at the heart of the clotting-related complications seen in long COVID patients.

Implications for Treatment

The study’s findings are not just theoretical; they offer a potential therapeutic solution. Researchers found that monoclonal antibodies, specifically targeting the spike protein, can prevent the formation of fibrin and therefore stop the clotting cascade. A particular monoclonal antibody, named 5B8, was shown to block the spike protein’s ability to bind to the blood vessel lining. This blockage prevented fibrin buildup, stopping further complications without affecting normal immune function.

This treatment option is particularly important as it avoids the blood clotting issues that have been linked with some COVID-19 vaccines, which also use spike proteins. Researchers were quick to clarify that the vaccine-related clotting problems stemmed from the adenovirus component of the vaccines and not from the spike protein itself.

Lack of Correlation Between Initial Severity and Long COVID

One of the significant findings of the study is the weak correlation between the initial severity of COVID-19 and the likelihood of developing long COVID. The research revealed that even patients who had mild or asymptomatic cases of COVID-19 could experience long-term effects due to fibrin buildup. This explains why blood thinners have not been universally effective in managing long COVID symptoms, as they do not address the root cause—excess fibrin production.

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Ongoing Questions and Future Research

While the study offers promising insights, it also leaves room for further investigation. Critics have pointed out that the study’s duration and mouse-model approach may not perfectly replicate human physiology. There is also a need for more extensive clinical trials to determine if this therapeutic strategy will hold up in human populations.

Moreover, questions remain about how long the fibrin accumulation lasts post-infection and why it continues even after the virus has been cleared from the system. The researchers noted that they are planning to conduct larger-scale human trials to confirm their findings.

Conclusion

This new understanding of long COVID provides hope for millions suffering from the condition. By identifying fibrin as the key driver behind post-COVID complications, researchers have opened the door to novel treatments that can prevent or reverse long COVID’s debilitating effects. With monoclonal antibody therapies showing promise in preclinical trials, there is optimism that an effective treatment for long COVID may be on the horizon.


[Source:- The Hindu]

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