Previously scientists have determined that entry of SARS-CoV-2 into cells occurs through a receptor on the cell surface, known as ACE2 but a new study has found that the ACE2 receptor is at very low levels in human lung tissue.
Researchers at McMaster University (MU) and the University of Waterloo in Canada are searching for how the SARS-CoV-2 virus infects the lungs – and they’re challenging what has become an accepted truth about the virus.
“Our finding is somewhat controversial, as it suggests that there must be other ways, other receptors for the virus, that regulate its infection of the lungs,” said study researcher Jeremy Hirota from MU.
“We were surprised that the fundamental characterization of the candidate receptors in human lung tissue had not yet been done in a systematic way with modern technologies,” Hirota added.
“Finding such low levels of ACE2 in lung tissue has important implications for how we think about this virus. ACE2 is not the full story and may be more relevant in other tissues such as the vascular system,” said study researcher Andrew Doxey from Waterloo.
To explore alternate additional infection pathways and different patient responses to infection, the team is using nasal swabs that were collected for clinical diagnoses of Covid-19, the study, published in the European Respiratory Journal, reported.
These samples offer the opportunity to determine which genes are expressed by patients’ cells and associate this information with the development of the patients’ disease.
The ongoing study will better identify and treat patients who are at risk of developing serious complications and provide predictive capacity for hospitals.
According to the researchers, It is clear that some individuals respond better than others to the same SARS-CoV-2 virus.
“The differential response to the same virus suggests that each individual patient, with their unique characteristics, heavily influences Covid-19 disease severity,” said Hirota.
“We think it is the lung immune system that differs between Covid-19 patients, and by understanding which patients’ lung immune systems are helpful and which are harmful, we may be able to help physicians proactively manage the most at risk-patients,” he noted.