Stopping fatal lung damage from influenza: MG53 protein shows promise in...

Stopping fatal lung damage from influenza: MG53 protein shows promise in...
Stopping fatal lung damage from influenza: MG53 protein shows promise in...
The raging pneumonia that can contribute to death from flu can be stopped with a drug made from a naturally occurring human protein, according to a new animal study.

In mouse studies, all untreated animals given a lethal dose of influenza died within a few days. All but one of the infected mice treated with the experimental therapy not only survived, but stayed energetic and maintained weight despite high levels of the flu virus in their lungs.

The experimental treatment is a heavy dose of MG53, part of a family of proteins that play an essential role in repairing cell membranes. MG53 has already been identified as a potential therapy for conditions ranging from Alzheimer’s to persistent skin wounds. In this study, MG53 was found to prevent death from fatal flu infection by blocking excessive inflammation – without affecting the virus itself.

The researchers are currently testing the effects of the therapy in mice infected with SARS-CoV-2, the coronavirus that causes COVID-19.

“I’ve never seen anything like it,” said Jacob Yount, associate professor of microbial infection and immunity at Ohio State University and co-lead author on the study. “Although these mice had the same viral load as the untreated mice, they didn’t get very sick – with the lethal dose of the flu.”

Yount, whose lab studies the immune response to viral infections, led the work with Jianjie Ma, professor of cardiac surgery at Ohio State, who discovered MG53 and its role in cell repair and developed the protein as a therapeutic.

For this new work, the scientists put MG53 on the test against influenza, which, along with other respiratory viruses, is one of the top 10 causes of death worldwide.

The researchers infected mice with a dose of an H1N1 strain of influenza and treated half with a placebo. Using recombinant human MG53, a molecule Ma’s laboratory developed as a drug, the researchers treated the other half of the mice with seven daily injections starting 24 hours after infection. The untreated mice showed aggressive weight loss and died within nine days, but 92% of the treated mice lost very little weight, remained active, and returned to normal weight two weeks after infection.

“The protein has a way of detecting injured tissue and getting there directly,” Ma said. “We’re basically improving a natural anti-inflammatory mechanism in the body so that the body can better defend itself when you’re facing an aggressive viral infection crisis.”

Despite the strikingly different results, the viral load was similar in both sets of mice – which means that an MG53-based drug is not an antiviral drug. Even when infected with the flu virus, the respiratory tracts of the treated mice showed only minor tissue damage.

Although the team is still working to fully identify how this protection occurs, the researchers found that MG53 stops an immune response mishap known as a “cytokine storm,” which is causing tissue damage. Research also showed that MG53 mitigates an infection-related cell death process called pyroptosis, which also promotes inflammation and lung dysfunction.

“Much of the lung damage with the flu virus is actually caused by excessive inflammation from our own immune response,” said Yount. “If you can dampen this hyperactive immune response, you will have less tissue damage, even though the virus is still replicating at a very high level.”

Lung tissue damaged by inflammation is fatal as fluid and cells build up in the airways and prevent the lungs from taking in oxygen.

Ma’s previous work on animal models suggests that it is safe to raise MG53 levels in the body for therapeutic purposes: mice that have been genetically engineered in his laboratory to overproduce the protein live longer and healthier than normal mice. Although scientists envision MG53 as part of a drug cocktail for deadly viral infections, they warn that much more research is needed before therapy is available to humans.

“We need better anti-inflammatory tissue repair therapies,” Ma said. “We don’t have COVID-19 data yet, but even with influenza, which affects us seasonally, this application could make a big difference.”

This work was supported by grants from the National Institutes of Health and the Department of Defense, and a presidential scholarship from Ohio State University.

Recombinant MG53 protein protects mice from deadly influenza virus infection. American Journal of Respiratory and intensive care medicine, October 8, 2020.

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