More than eight months after the World Health Organization (WHO) declared COVID-19 as a global pandemic, the disease is far from being under control with several countries experiencing a stronger second wave. One common factor that has been observed across the world is that the coronavirus predominantly affects adults and older people while sparing children. Now, scientists in the US have found an explanation for this.
Researchers from Vanderbilt University Medical Center (VUMC) and some other institutes say that children have lower levels of a receptor protein that the coronavirus SARS-CoV-2 needs to invade airway epithelial cells in the lung, the Hindustan Times reported.
Published in the Journal of Clinical Investigation, the findings of the study support efforts to block this protein to treat or prevent COVID-19 in older people.
“Our study provides a biologic rationale for why particularly infants and very young children seem to be less likely to either get infected or to have severe disease symptoms,” said Jennifer Sucre, a co-author of the study from VUMC.
According to the researchers, once a viral particle is inhaled into the lungs, protein ‘spikes’ attach to ACE2, a receptor on surfaces of some lung cells.
Another cellular protein called TMPRSS2 enables the virus to fuse into the cell membrane and break into the cell. “Our research has always focused on understanding lung development and how infant lungs differ from adult lungs in their vulnerability to injury,” Sucre said.
“In this study we actually took the opposite approach, and were able to see how developing lung by its differences is protected from SARS-CoV-2 infection,” she added.
The scientists used a technique called ‘single-cell RNA-sequencing’ to detect the expression of genes in individual mice cells of tissues like the lung.
“While gene for ACE2 was expressed at low levels in the mouse lung, TMPRSS2 stood out as having a really striking trajectory of increased expression during development,” said Bryce Schuler, a co-author of the study.
They analyzed human lung specimens collected from donors of different ages, and confirmed that trajectory in TMPRSS2 expression was similar to what they found in mice.