The current CoVID-19 pandemic has thrown the world health systems and socioeconomic status into chaos. Devaux, Rolain, Colson and Raoult (2020) have proposed repurposing of chloroquine as an antiviral drug against SARS-CoV-2 virus which is believed to cause CoVID-19 disease in humans. In my opinion, this proposition is relevant and justified.

In the introduction, the authors critically outlined the clinical history of chloroquine as an antimalarial drug; its efficacy, prophylaxis and pharmacokinetics. The authors also explained the similarities and differences between chloroquine and hydroxychloroquine. The efficacy of chloroquine as an antimalarial drug gradually declined due to emergency of chloroquine-resistant P. falciparum strains. It was worthy highlighting the broad spectrum activity of chloroquine against bacteria, fungi and viruses. In this regard, I believe the introduction captured all vital details.

Devaux, et al. (2020), indicated with supporting evidence, the in vitro antiviral potential of chloroquine against RNA viruses such as HIV, rabies virus, hepatitis A virus, hepatitis C virus, influenza A and B viruses, influenza A H5N1 virus, polio virus, Dengue virus, Lassa virus, Chikungunya virus, Zika virus, Hendra and Nipah virus and Ebola virus; besides DNA viruses such as herpes simplex virus and hepatitis B virus. The authors also mentioned the promising in vitro potential of chloroquine against coronaviruses: SARS-CoV-1, MERS-CoV, HCoV-229E and HCoV-O43 as reported in past studies. While I wholly agree with the results on the antiviral potential of chloroquine, I strongly believe the authors would have provided reported numerical data such as rate of risk, therapeutic data, recovery rate, infection rate and mortality rate. Additionally, in vivo antiviral potential of chloroquine should have been provided. More data on antiviral activity on coronaviruses in particular ought to have been given.The mechanisms of action of chloroquine against various viruses as reported in past studies were well discussed by Devaux, et al. (2020).

Based on past research, the authors identified several modes of action; namely,

1. Inhibition of quinone reductase 2 that is involved in the biosynthesis of sialic acids. The broad antiviral spectrum activity of chloroquine is thought to be associated with its interference with sialic acid,

2. Impairement of virus replication by interfering with the pH- dependent endosome- mediated entry of enveloped viruses,

3. Interference with post- translational modification of viral proteins,

4. Interference with the normal proteolytic processing of the flavivirus prM protein to M protein,

5. Inhibition of budding with accumulation of noninfectious particles,

6. Cell signaling and regulation of pro-inflammation cytokines,

7. Inhibition of phosphorylation of the p38 mitogen- activated protein kinase (MAPK) in THP-1 cell and Caspase,

8. Activation of anti-SARS-CoV-2 CD8*T- cells to elicit a broad protective immune system.

The mechanisms are well outlined supported by references. Hypothetical diagrams could have been used to simplify the modes of action.

The conclusion is clear and it summarizes the entire article; although, I feel hypothetical mode of action of chloroquine against SARS-CoV-2 should have been put under the mode of action section. This article is concise, relevant and justified. I therefore approve it with minimal modifications.