Using 'mini-lungs,' scientists find that more types of lung cells can be infected by SARS-CoV-2 than previously thought

Scientists at Sanford Burnham Prebys, University of California San Diego and their international collaborators have reported that more types of lung cells can be infected by SARS-CoV-2 than previously thought, including those without known viral receptors, reports News Medical.

The research team also reported for the first time that the lung is capable of independently mustering an inflammatory antiviral response without help from the immune system when exposed to SARS-CoV-2.

Scientists reported their new discoveries about SARS-CoV-2 and COVID-19 in a paper published, in Proceedings of the National Academy of Sciences.

The scientists used a technique to transform cells taken from patients into cells resembling stem cells. These embryonic-like cells-;known as induced pluripotent stem cells (iPSCs)-;can then be turned into other types of human cells. The team caused them to develop into a grouping of various lung cell types in a pattern that mimics the human lung at a smaller scale.

"With most models for studying respiratory infections, you can't isolate a specific cellular response because you have all the immune system cells rushing in to help deal with the invaders,” the authors of the study noted.

“Using our lung organoids or 'mini lungs,' another benefit is that we can choose the sex of the cells so we're not just studying male-dominant or female-dominant lung tissue. This is important, as we know that the lung responds differently during disease if you're a female or a male," they added.

The scientists observed that SARS-CoV-2 was able to acutely infect many previously undescribed cell types in the mini lungs. This held true when testing different strains of SARS-CoV-2, although it was clear that certain strains were more effective at infecting specific cell types.

"People used to say that SARS-CoV-2 only infects cells with certain receptors, especially those with the ACE2 receptor known to interact with the infamous SARS-CoV-2 spike protein. We demonstrated that when a direct entry point was unavailable, the virus just punches through the cell membrane instead," the scientists emphasize.

"With the Delta variant having produced more severe symptoms, and the Omicron variant being less deadly but more contagious, we hypothesized that Delta may prefer the alveolar cells deeper in the lungs, while Omicron sticks more to the upper airways. While all strains were capable of infecting many lung cell types, we did see a distinct preference for these strains, as predicted," the study authors note.

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