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Sulforaphane exhibits antiviral activity against pandemic SARS-CoV-2 and seasonal HCoV-OC43 coronaviruses in vitro and in mice

Alvaro A. Ordoñez, C. Korin Bullen, A.F. Villabona-Rueda, Elizabeth A. Thompson, Mitchell L. Turner, Vanessa F. Merino, Yu Yan, John Kim, S. Lindsey Davis, Oliver Komm, Jonathan D. Powell, Franco R. D’Alessio, Robert H. Yolken, Sanjay K. Jain, Lorraine Jones‐Brando

2022Communications Biology82 citationsDOIOpen Access PDF

Abstract

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), has incited a global health crisis. Currently, there are limited therapeutic options for the prevention and treatment of SARS-CoV-2 infections. We evaluated the antiviral activity of sulforaphane (SFN), the principal biologically active phytochemical derived from glucoraphanin, the naturally occurring precursor present in high concentrations in cruciferous vegetables. SFN inhibited in vitro replication of six strains of SARS-CoV-2, including Delta and Omicron, as well as that of the seasonal coronavirus HCoV-OC43. Further, SFN and remdesivir interacted synergistically to inhibit coronavirus infection in vitro. Prophylactic administration of SFN to K18-hACE2 mice prior to intranasal SARS-CoV-2 infection significantly decreased the viral load in the lungs and upper respiratory tract and reduced lung injury and pulmonary pathology compared to untreated infected mice. SFN treatment diminished immune cell activation in the lungs, including significantly lower recruitment of myeloid cells and a reduction in T cell activation and cytokine production. Our results suggest that SFN should be explored as a potential agent for the prevention or treatment of coronavirus infections.

Topics & Concepts

SulforaphaneCoronavirusVirologyIn vitroImmunologyBiologyMedicineCoronavirus disease 2019 (COVID-19)DiseaseCancer researchInternal medicineInfectious disease (medical specialty)BiochemistryGenomics, phytochemicals, and oxidative stressVitamin C and Antioxidants ResearchDrug-Induced Hepatotoxicity and Protection