into the brain, causing a disorder known as influenza-associated encephalopathy (IAE). Researchers have discovered that the virus can enter the brain through endothelial cells in the blood. They found that viral proteins build up in these cells, suggesting that antiviral medications targeting viral transcription/translation could be helpful in treating some patients. This discovery is significant as there are currently limited treatment options for IAE, and it has the potential to improve patient care and reduce the number of IAE-related deaths globally.
The influenza virus can make its way to the brain and cause severe symptoms or even death in a condition called influenza-associated encephalopathy (IAE). Researchers have found that the virus may enter the brain through a specific type of cell, and they have also identified potential treatment methods. Despite the increasing prevalence of IAE, there is limited understanding of how the influenza virus penetrates the brain and leads to encephalopathy symptoms. Additionally, there is currently no definitive treatment for IAE. The study published in Acta Neuropathologica shed light on these issues.
Researchers from Osaka University wanted to investigate the connection between influenza viruses and acute encephalopathy (IAE).
In order to examine the potential causes of IAE, the research team utilized various methods. They examined virus particles in the brains of individuals who had died from IAE, developed a mouse model of the disease by introducing influenza A virus into the bloodstream, and utilized cell culture techniques to observe the virus’s ability to infect different types of cells.
“In the human brains, the virus-injected mice, and the cultured cells, the influenza virus tended to accumulate in endothelial cells,” stated lead author Shihoko Kimura-Ohba. “These cells play a crucial role in creating a barrier between the blood and the brain is crucial for protecting the brain from harmful substances,” the researchers stated. In both human brains and the mouse model, the barrier was found to be compromised. Instead of reproducing within these endothelial cells, the virus was observed to generate a large amount of proteins. “The accumulation of viral proteins in the brain led us to the realization that antiviral drugs targeting viral proliferation were unlikely to be effective,” explained Tomonori Kimura, the senior author of the study. He also stated that antivirals focused on a different aspect of the virus may be more beneficial.
The stopping of viral transcription and translation, which are important processes for making proteins, is also possible through the use of certain classes of antivirals.”
During experiments on endothelial cells treated with influenza virus, the team found that the use of these antivirals led to a decrease in viral proteins and cell death. In a mouse model of IAE, these antivirals proved to be highly effective when administered early, indicating their potential usefulness in human patients.
Since various viruses, including COVID-19, can cause encephalopathy, these findings have significant implications. Additionally, despite improvements in IAE care, more than half of all patients still die or suffer from long-lasting symptoms.An improved understanding of how viruses can lead to encephalopathy is crucial for the development of effective new treatments.
