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Authors: Emily Mantlo et al.

Link to paper:

Journal/ Pre-Print: bioRxiv

Key Words: SARS-CoV-2; COVID-19; Interferon; antiviral therapy; innate immune

Research Highlights 

1. Study of growth kinetics of SARS-CoV-2 in cultured cells (Vero cells)

2. SARS-CoV-2 replication is inhibited by IFN-α and IFN-β

3. Therapeutic potency of type I IFNs for COVID-19


In this study SARS-CoV-2 infection and its potential treatment with Type I interferons was studied in vitro. Growth kinetics of SARS-CoV-2 were characterized, and it was observed that viral titres peaked at approximatley 24 hours post-infection and remained stable until 40 hours post-infection. Cells were treated with IFN-α or IFN-β prior to infection and treatment was continued afterwards. With increasing IFN concentrations, the virus titres steadily decreased, with IFN-β being slightly more effective than IFN-α. The paper adds to the current knowledge on potential treatments, however, on a very fundamental level of research and not translational to the clinical use yet.

Impact for SARS-CoV2/COVID19 research efforts 

Understand the immune response to SARS-CoV2/COVID19

Understand the virology and/or cell biology of SARS-CoV2/COVID19

Potential for a new treatment option for SARS-CoV2/COVID19

Study Type

· In vitro study

Strengths and limitations of the paper

Novelty: New insights for using Type I IFN as potential treatment

Standing in the field: Results are not controversial and theoretically expected. Additionally, other preprint articles also show SARs-CoV-2 is susceptible to type I interferon inhibition.

Appropriate statistics: Yes

Viral model used: SARS-CoV-2 (USA-WA1/2020)

Translatability: Yes, but more clinical studies needed.

Main limitations:

The authors claim that SARS- CoV-2 is more susceptible to IFN than SARS-CoV, but they do not produce all the data needed to support this. EC50 values of both viruses would need to be determined in parallel in the same model system. It is claimed that Type I IFN is suppressing SARS-CoV-2 infection which could potentially be used for clinical treatment of patients. However, in all experiments the cells were already treated with IFN prior to infection not during. They also do not consider the proinflammatory properties of type I interferon. This is particularly important as pathology, in some patients, is thought to be driven by a cytokine storm to which IFNs can contribute.