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Scientists find a new way that prevents lung damage and death in SARS-CoV-2 infected

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New findings, published in the Arteriosclerosis, Thrombosis, and Vascular Biology, revealed a drug used to treat autoimmune diseases helped prevent lung damage and death in SARS-CoV-2 infected mice.

Their findings show that inflammatory lung vascular leakage, sometimes known as leaky lungs, is a critical hallmark of COVID-19 disease. Severe inflammation can produce vascular leakage, which results in an accumulation of fluid in the lungs, interfering with oxygen intake. Mice infected with SARS-CoV-2 displayed very evident and early indications of pulmonary blood vessel leaking.

The study also suggests that targeted drug treatments that suppress only specific immune system pathways, such as the rheumatoid arthritis drug used in the study, which targets the molecular receptor called IL-1, may be a better option for COVID-19 patients than drug treatments that suppress the entire immune system.

In the study, the researchers monitored and tracked the progression of disease in mice infected with the virus. They observed that the mice rapidly developed symptoms such as weight loss, fluid accumulation in the lungs due to leaky lung blood vessels, and even signs of lung scarring, such as elevated collagen levels in lung tissue.

“This is important evidence that blood vessel leakage in the lungs is a key feature of severe COVID-19 and that treatments which prevent or reduce vascular leakage warrant further study,” said co-senior author Jalees Rehman.

Additionally, the researchers administered an approved autoimmune illness medicine called anakinra to some of the animals to inhibit the IL-1 receptor, a critical protein regulating inflammation.

“We saw that the mice who received the drug had reduced signs of disease—including less lung fluid buildup and less scarring of the lungs—and better survival,” said the co-author.

According to Rehman, these findings pave the way for treating COVID-19 patients and highlight the importance of more research into focused, individualized therapy.

“Obviously, the best approach to reducing short-term and long-term damage as a result of COVID-19 is to get vaccinated and reduce the risk of SARS-CoV-2 infection as well as the risk of severe disease. However, the hesitancy of many individuals to get vaccinated as well as the lack of access to vaccines in many parts of the world means that we will continue to see patients with severe COVID-19 in the near future. Our results suggest that it is possible to identify a select a vulnerable COVID-19 patient population that is most likely to benefit from this therapy,” Rehman added.

The researchers hypothesize that by assessing the level of specific inflammatory signals in patients, such as activation of the IL-1 receptor pathway, they will be able to determine when a patient’s immune system is going into overdrive and use a targeted immunosuppressant, such as anakinra, to maintain the proper balance of inflammation.

“It is important to get the right drug to the right patient at the right time, and this study shines a light on a path forward for clinical trials that are investigating this drug and others that target specific components of the immune system,” Rehman concluded.

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