Detecting mechanism of causing respiratory disease in children

US scientists at the University of Texas have identified a mechanism that causes one of the most common and dangerous infections in children, respiratory diseases.

The results of this study were published in the March issue of the American Journal of Respiratory and Critical Care Medicine.

Picture 1 of Detecting mechanism of causing respiratory disease in children

By analyzing blood samples from newborns with respiratory infections and data from mouse experiments, the scientists determined that the respiratory syncytial virus (RSV) had prevented the ability of respiratory cells to produce enzymes that help control susceptible molecules (reactive oxygen species).

RSV interferes with this process by preventing the activation of a single protein that plays a role in the activity of detoxifying enzymes. The reactive oxygen then accumulates, causing oxidative stress and inflammation in the respiratory cells that have not been affected.

Dr. Antonella Casola said that the role of oxidative stress has been mentioned in previous studies, but this is the first study of the link between lung infection and viral infection.

Previously, American scientists at the Jewish National Health Center in Denver also found a naturally occurring POPG lipid compound in the alveoli of the human lung. Scientists tested the effect of POPG on human lung cells and RSV-infected mice.

The results showed that the POPG-protected cells before exposure to the virus were less likely to be infected, the inflamed cells were less likely to enter the lungs. This finding may also open new directions in preventing and treating RSV infection.

The respiratory syncytial virus is a kind of refuge and waits for the opportunity to return to the same attack as the HIV and virus viruses that cause liver disease. Respiratory syncytial virus is quite common, most children are infected in the first year. About 40% of children develop bronchiolitis can return and more than one third can develop asthma.