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Studying SARS-CoV-2 using human lung organoids

3 August 2020
Appeared in BioNews 1058

Scientists from Stanford University, California, USA have developed a new model system to better study the lung damage that occurs during COVID-19. 

COVID-19, the disease caused by SARS-CoV-2, is known to primarily affect the lung tissue of infected individuals, often causing severe tissue damage that leads to critical pneumonia and acute respiratory distress syndrome (ARDS).

In the past scientists have struggled to study lung tissue because of difficulties in culturing the stem cells that give rise to two different lung cell types involved in lung healing after tissue damage: secretory club (AT1) cells and alveolar (AT2) cells. The researchers developed a way of culturing these cells without the difficulty of so-called 'feeder cells' previously thought essential to maintaining this culture.

To avoid these complications the researchers developed 3D lung organoids in which AT1 and AT2 cells grew well and were able to differentiate and self-renew. Importantly, they also engineered their organoids in such a way that their surface area contained the ACE2 receptors, which are the entry sites for SARS-CoV-2 into the cell. They then infected the cells with either the influenza virus or SARS-CoV-2 and tested if treatment with various drugs had an effect on viral infection. 

In addition to this study using organoids to study the effect of COVID-19 on lungs, several other labs have been using other types of organoids as tools to study the disease and its effect on brain cells, liver tissue and blood vessels. Some scientists even started 3D bio-printing of miniature organs and human tissue to study the effects of the virus. 

Dr Anthony Atala, director of the Wake Forest Institute for Regenerative Medicine whose lab is printing human tissue to test drugs for COVID-19, told the New York Times that the organoids allow researchers to analyse a drug's impact on an organ. 'We never thought we'd be considering this for a pandemic,' he said.

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