Antimalarial drugs inhibit the replication of SARS-CoV-2: An in vitro evaluation

In December 2019, a new severe acute respiratory syndrome coronavirus (SARS-CoV-2) causing coronavirus diseases 2019 (COVID-19) emerged in Wuhan, China. African countries see slower dynamic of COVID-19 cases and deaths. One of the assumptions that may explain this later emergence in Africa, and more particularly in malaria endemic areas, would be the use of antimalarial drugs. We investigated the in vitro antiviral activity against SARS-CoV-2 of several antimalarial drugs. Chloroquine (EC₅₀ = 2.1 μM and EC₉₀ = 3.8 μM), hydroxychloroquine (EC₅₀ = 1.5 μM and EC₉₀ = 3.0 μM), ferroquine (EC₅₀ = 1.5 μM and EC₉₀ = 2.4 μM), desethylamodiaquine (EC₅₀ = 0.52 μM and EC₉₀ = 1.9 μM), mefloquine (EC₅₀ = 1.8 μM and EC₉₀ = 8.1 μM), pyronaridine (EC₅₀ = 0.72 μM and EC₉₀ = 0.75 μM) and quinine (EC₅₀ = 10.7 μM and EC₉₀ = 38.8 μM) showed in vitro antiviral effective activity with IC₅₀ and IC₉₀ compatible with drug oral uptake at doses commonly administered in malaria treatment. The ratio C_lung/EC₉₀ ranged from 5 to 59. Lumefantrine, piperaquine and dihydroartemisinin had IC₅₀ and IC₉₀ too high to be compatible with expected plasma concentrations (ratio C_max/EC₉₀ < 0.05). Based on our results, we would expect that countries which commonly use artesunate-amodiaquine or artesunate-mefloquine report fewer cases and deaths than those using artemether-lumefantrine or dihydroartemisinin-piperaquine. It could be necessary now to compare the antimalarial use and the dynamics of COVID-19 country by country to confirm this hypothesis.