The transmission electron micrograph shows a virus. Credit: CDC.
The body's exaggerated inflammatory response to respiratory viruses, including the one that causes COVID-19, could be deterred by one viralprotein.
The human body's immune response can destroy the respiratory syncytial virus if it lacks the viral protein, according to a study. The research was published in the journal mBio.
Respiratory viruses like the COVID-19-causing SARS-CoV-2 virus and theRSV are similar in that they use lung cells as factories to make more viruses. These cells are prone to multiplication of Viruses that cause inflammation, lung diseases, and sometimes death.
Kim Chiok, a post-doctoral researcher at Washington State University, said that exaggerated inflammation makes breathing difficult. People with long-term and severe inflammatory responses end up in the hospital because they get pneumonia and need help breathing.
Chiok and his colleagues at the University of Washington are trying to break the cycle by understanding how respiratory viruses persist in the cell. According to the National Institute of Allergy and Infectious Diseases, the majority of deaths from the disease are in infants, children, elderly and immune-compromised individuals.
Professor Santanu Bose is a part of the Veterinary Microbiology and Pathology research unit. Chiok, who was a Fulbright Scholar from Peru, spent the past two and a half years in the Bose laboratory researching the mechanisms that regulate the virus-host battle.
The researchers first determined the functions of the viral genes by using viruses without genes that code for different viral genes and comparing them to a wild strain of the virus.
Chiok said they wanted to learn about the tools the virus has by taking them away.
Each tool has a different viralprotein.
Chiok found that the viral NS2 is a key regulator of autophagy, a cellular process that affects immune defense during virus infections. The autophagy is caused by a cellularprotein.
The threat from the cell can be cleared by Beclin1 when the virus enters the cell. It does this by attaching to small genes through a process called ISGylation. Chiok said it is almost like a suit of armor.
The study showed that the virus can persist and replicate within the cell, spreading to other cells and causing damage that leads to airway diseases such as pneumonia. The virus is destroyed by Beclin1 without the NS2 protein.
Chiok said that disabling the ability of NS2 to modify the cell's immune defense mechanism is a way to do that. "You can use drugs to target thatProtein, and potentially transfer that concept to other respiratory Viruses like Influenza A virus and the Severe Acute Respiratory Syndrome-CoV-2."
The human respiratory syncytial virus NS2 is induces autophagy. There is a DOI: 10128/mbio.03528-21.
The journal has information about mBio.
Respiratory Viruses that hijack immune mechanisms may have a new name.
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