Virus protein undermines protective mechanism of cells
Respiratory viruses such as the SARS-CoV-2 coronavirus, human respiratory syncytial virus (RSV) and influenza viruses can cause severe inflammatory reactions in the body. According to a recent study, these viruses have a protein that protects them from the natural defense mechanisms of human cells. However, this protein could also represent a common vulnerability.
Researchers at Washington State University’s College of Veterinary Medicine (USA) have discovered a potential vulnerability shared by respiratory viruses that override immune mechanisms. According to the current study, a protein that the virus uses to protect itself from the body’s immune system represents a promising target. The research results were recently published in the journal “Race” presents.
Respiratory viruses can cause severe inflammation
Many respiratory viruses such as SARS-CoV-2, influenza and RSV infect the lung cells responsible for gas exchange and then use these as factories to produce other viruses. The uncontrolled virus multiplication in these cells leads to their destruction and can lead to serious complications such as pneumonia, which in the worst case can lead to death.
“High levels of inflammation clog the airways and make it difficult to breathe,” said study leader Kim Chiok of Washington State University. That is the reason why people who suffer from long-term inflammatory reactions in the lungs get pneumonia and, in particularly severe cases, end up in an intensive care unit and have to be artificially ventilated.
One protein seems to make the difference
Chiok’s working group discovered in RS viruses that a virus protein called NS2 can provide information about the risk of a strong inflammatory reaction in the body after an infection. Apparently, the lung cells are better able to destroy the virus before an excessive inflammatory response occurs when the protein is absent.
NS2 protects the virus from autophagy
According to the researchers, the RS virus uses the NS2 protein to protect itself from the effects of autophagy, a process in which cells break down their own components to dispose of misfolded proteins and other pollutants. After the virus enters the host, the cell uses autophagy to try to destroy it.
Chiok’s team identified the viral NS2 protein as an important regulator that protects the virus from autophagy. Cells mediate internal defenses via a protein called Beclin1. This ensures that parts inside the cell are protected from the virus. However, the NS2 protein removes this protection again and thus prevents the cell’s protective measures from taking effect.
According to the working group, this allows the virus to survive inside the cell, multiply and spread to other cells, triggering an inflammatory response in the body that can culminate in pneumonia. The researchers were able to show that RS viruses without NS2 are routinely destroyed by Beclin1. “In a way, you turn off NS2’s ability to modulate the cell’s immune defense mechanism,” explains Chiok.
Approach for new therapies against respiratory viruses
“One could use therapeutics that target this protein and possibly transfer this concept to other respiratory viruses such as the influenza A virus and SARS-CoV-2,” summarizes the study leader. The findings lay the groundwork for breaking the cycle by which respiratory viruses overturn cellular defenses. (vb)
Author and source information
This text corresponds to the specifications of medical specialist literature, medical guidelines and current studies and has been checked by medical professionals.
Diploma-Editor (FH) Volker Blasek
- Washington State University: Respiratory viruses that hijack immune mechanisms may have Achilles’ heel (veröffentlicht: 18.01.2022), news.wsu.edu
- Kim Chiok, Swechha M. Pokharel, Indira Mohanty, et al.: Human Respiratory Syncytial Virus NS2 Protein Induces Autophagy by Modulating Beclin1 Protein Stabilization and ISGylation; in: mBio, 2022., journals.asm.org
This article contains general advice only and should not be used for self-diagnosis or treatment. He can not substitute a visit at the doctor.