A new study by Washington State University researchers could hold the key to treating respiratory viruses, including RSV and coronaviruses like the one that causes COVID-19.
The research, led by post-doctoral student Kim Chiok, found a relationship between an RSV virus protein and a respiratory cell protein that could explain part of the inflammation that occurs as a result of a respiratory virus entering the lungs and respiratory tract. The research was published last month in the journal mBio.
The team isolated the respiratory syncytial virus, known as RSV, which impacts both infants and older adults the most, leading to hospitalization and sometimes death.
Every year in the United States, RSV leads to 58,000 hospitalizations of children younger than 5 and accounts for 14,000 deaths in adults 65 and older, according to the Centers for Disease Control and Prevention.
To understand the significance of the team’s findings, it’s important to understand how respiratory viruses infect cells and cause inflammation.
When respiratory viruses work their way into the lungs, they infect the cells that are in charge of exchanging oxygen. The virus infects the cells, replicates itself and manipulates the immune system, which is trying to control the damage it detects.
Respiratory viruses have different proteins that can manipulate our immune response, and in the case of RSV, those proteins can cause excess inflammation, making it challenging for the immune response to combat the virus.
Chiok and her team were studying a specific viral protein of RSV, called NS2, and its relationship to another protein located in our respiratory cells.
When RSV infiltrates cells, it starts producing NS2 very early in the process, which enables the virus to manipulate the body’s immune response.
The WSU study is the first to identify the relationship between NS2 and a protein inside our respiratory cells, called Beclin1. The study found that when the virus’s NS2 proteins come into contact with Beclin1, the interaction exaggerates some of the Beclin1’s functions, which include inflammation.
Beclin1 is a part of how inflammation occurs in our bodies, and is an essential component of autophagy, the mechanism by which our bodies can control aspects of our immune response, Chiok said.
If Beclin1 interacting with viral proteins plays a key role in how inflammation occurs when we get respiratory viruses, future research could target treatment to that protein in our respiratory cells, since we all have them. And while the NS2 protein is specific to RSV, all respiratory viruses contain proteins, Chiok said.
“You have nonstructural proteins in all viruses and the same process occurring in all respiratory cells,” Chiok said. “And while our study only looks at RSV, we need to take a step back and look at whether this mechanism occurs – and it probably occurs – in other respiratory viruses, like COVID or influenza, because all of them follow the same pathology once they’re in the lungs.”
Ideally, therapeutics could target the interaction or relationship between viral proteins and Beclin1 protein to taper down the inflammatory responses, Chiok added.
“Because we are all the same, therapeutics toward that human side can help us all against viruses that follow very similar pathways, like pneumonia-causing viruses,” Chiok said.