IMR Press / FBL / Volume 27 / Issue 1 / DOI: 10.31083/j.fbl2701003
Open Access Original Research
UV-4B potently inhibits replication of multiple SARS-CoV-2 strains in clinically relevant human cell lines
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1 Department of Medicine, Institute for Therapeutic Innovation, College of Medicine, University of Florida, Orlando, FL 32827, USA
2 Department of Pharmaceutics, College of Pharmacy, University of Florida, Orlando, FL 32827, USA
3 Emergent BioSolutions, Gaithersburg, MD 20879, USA

Academic Editor: Sang Heui Seo

Front. Biosci. (Landmark Ed) 2022, 27(1), 3;
Submitted: 26 October 2021 | Revised: 10 December 2021 | Accepted: 17 December 2021 | Published: 5 January 2022
(This article belongs to the Special Issue Vaccine and anti-viral drug development for SARS-CoV2)
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Background: SARS-CoV-2 is the coronavirus responsible for the COVID-19 pandemic. Although it poses a substantial public health threat, antiviral regimens against SARS-CoV-2 remain scarce. Here, we evaluated the antiviral potential of UV-4B, a host targeting antiviral, against SARS-CoV-2 in clinically relevant human cell lines. Methods: Cells derived from human lung (A549 cells transfected with human angiotensin converting enzyme 2 receptor (ACE2; ACE2-A549)) and colon (Caco-2) were infected with either a wild type or beta variant strain of SARS-CoV-2 and exposed to various concentrations of UV-4B. Supernatant was sampled daily and viral burden was quantified by plaque assay on Vero E6 cells. Results: Therapeutically feasible concentrations of UV-4B inhibited the replication of the wild type strain in ACE2-A549 and Caco-2 cells yielding EC50 values of 2.694 and 2.489 μM, respectively. UV-4B’s antiviral effect was also robust against the beta variant in both cell lines (ACE2-A549 EC50: 4.369 μM; Caco-2 EC50: 6.816 μM). Conclusions: These results highlight UV-4B’s antiviral potential against several strains of SARS-CoV-2.

Host targeting
Fig. 1.
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