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Reference #a549-hace2tpsa-av can only be ordered together with reference #a549-hace2tpsa.

A549 lung carcinoma cells expressing the SARS-CoV-2 receptors ACE2 and TMPRSS2

Permissivity of A549-hACE2 and A549-hACE2-TMPRSS2 cells to SARS-CoV-2 infection

InvivoGen offers human A549 lung carcinoma cell lines, specifically designed for COVID-19 studies:

— A549-hACE2 cells
— A549-hACE2-TMPRSS2 cells

These cells stably overexpress the genes encoding for the SARS-CoV-2 receptors, human ACE2, and TMPRSS2.

More details

The A549 cell line is commonly used for the study of respiratory infections. SARS-CoV-2, the causative agent of coronavirus disease-19 (COVID-19), gains entry into the human lung epithelium through the interaction of the virus Spike protein with the host ACE2 and TMPRSS2 receptors [1, 2]. A549 cells express negligible levels of ACE2 and no TMPRSS2 and thus are poorly permissive to infection by SARS-CoV-2 or Spike pseudotyped lentiviral particles [1-3, in-house data]. To increase their permissivity, A549 cells have been stably transfected with the human ACE2 only, or ACE2 and TMPRSS2 genes. In contrast to A549 cells, A549-hACE2 cells are permissive to Spike pseudotyped lentiviral particles as visualized by the expression of the lentiviral GFP transgene. The addition of TMPRSS2 expression significantly increases the cell line infectivity (see Figures).

Key features:

Overexpression of human ACE2 only, or ACE2 and TMPRSS2
Permissive to SARS-CoV-2 Spike pseudotyped lentiviral particles

Applications:

Screening of small molecule inhibitors and/or neutralizing antibodies of the ACE2‑Spike interaction
Screening of small molecule inhibitors and/or neutralizing antibodies of the TMPRSS2 surface protease
Comparative studies of the effects of drugs targeting ACE2 and/or TMPRSS2 on the SARS-CoV-2 infection and cellular signaling outcomes

Learn more about SARS-CoV-2 infection cycle, immune responses, and potential therapeutics.

References

1. Chen H. et al., 2020. SARS-CoV-2 activated lung epithelia cell proinflammatory signaling and leads to immune dysregulation in COVID-19 patients by single-cell sequencing. medRxiv: DOI 10.1101/2020.05.08.20096024.
2. Hoffmann M. et al., 2020. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 181:1-16.
3. Matsuyama S. et al., 2020. Enhanced isolation of SARS-CoV-2 by TMPRSS2-expressing cells. PNAS. 117(13):7001-7003.

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