COVID-19-Related Cell Lines

Designed for studying SARS-CoV-2 & developing therapeutics

InvivoGen has developed families of cell lines, derived from the human embryonic kidney 293 (HEK-293) cell line or the human A549 lung carcinoma cell line, to aid in your COVID-19 related research. They have been specifically designed to study SARS-CoV-2 infection, as well as for the development of novel therapeutics, targeting either the virus or the subsequent pro-inflammatory immune response.  


ACE2-(TMPRSS2) expressing cells

InvivoGen's COVID-19 related cell lines
InvivoGen's various families of COVID-19-related cell lines

These cells express high levels of the host receptor ACE2 alone, or in combination with the host protease TMPRSS2, at their cell surface. Thus, these cells are permissive to infection by SARS-CoV-2 Spike-pseudotyped lentiviral particles [1-3]. These cells either express MDA5 (Melanoma Differentiation Associated gene 5) and RIG-I (Retinoic Acid Inducible protein 1) endogenously or are knockout for each gene, individually. MDA5 and RIG-I are sensors of viral RNA that have been reported to participate in the immune response to SARS-CoV-2 infection [4-6]. Of note, the addition of TMPRSS2 in A549 cells only significantly increases their infectivity [in-house data]. This cell line collection is ideal for screening small molecule inhibitors and neutralizing antibodies that aim to block the virus-host interaction and cellular signaling outcomes [4-7].

Type I IFN reporter cells

These cells express an interferon regulatory factor (IRF)-inducible reporter and thus are ideal for studying how various SARS-CoV-2 proteins, such as the non‑structural proteins (NSPs), interfere with the anti‑viral interferon (IFN) response [8]. 

Pro-inflammatory cytokine reporter cells

These cells feature a fully functional signaling pathway that is specific for IL‑6, IL‑1β, or TNF‑α. They can be used to investigate ways to block the signaling pathways induced by these cytokines, which are associated with the hyper-inflammatory response triggered by SARS-CoV-2 in the more severe cases of infection [9].




1. Crawford, K.H.D. et al. 2020. Protocol and Reagents for Pseudotyping Lentiviral Particles with SARS-CoV-2 Spike Protein for Neutralization Assays. Viruses 12 (5):513
2. Daniloski, Z. et al. 2020. The Spike D614G mutation increases SARS-CoV-2 infection of multiple human cell types. bioRxiv. doi:10.1101/2020.06.14.151357
3. 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.
4. Ying X. et al., 2021. MDA5 governs the innate immune response to SARS-CoV-2 in lung epithelial cells. Cell Reports. 34:108628.
5. Rebendenne A. et al., 2021. SARS-CoV-2 triggers MDA-5-dependent interferon response which is unable to control replication in lung epithelial cells. J. Virol. doi:10.1128/JVI.02415-20.
6. Wu J, et al., 2021. SARS-CoV-2 ORF9b inhibits RIG-I MAVS antiviral signaling by interrupting K63-linked ubiquitination of NEMO. Cell Reports. 34(7):108761.
7. Hu, J. et al. 2020. Development of cell-based pseudovirus entry assay to identify potential viral entry inhibitors and neutralizing antibodies against SARS-CoV-2. Genes Dis. doi:10.1016/j.gendis.2020.07.006
8. Banerjee, A.K. et al. 2020. SARS-CoV-2 Disrupts Splicing, Translation, and Protein Trafficking to Suppress Host Defenses. Cell. doi:10.1016/j.cell.2020.10.004
9. Del Valle, D.M. et al. 2020. An inflammatory cytokine signature predicts COVID-19 severity and survival. Nat Med 26, 1636-1643.

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