Figure 5  Proposed mechanism for Hydroxychloroquine (HCQ) antiviral activity against COVID-19 and HIV. HCQ seems to block the virus’ entry into the cell by preventing the binding of viruses to the cell surface receptor and increasing the phagolysosome pH, thus interrupting the virus fusion to the host cells. HCQ can also inhibit nucleic acid replication, viral proteins glycosylation, virus assembly, transport of new virus particles, viruses release, and other processes to achieve its antiviral effects [14]. Specifically, the anti-HIV activities are highly linked to the post-translational modification of glycoprotein 120 (gp120). This leads to the loss of gp120 immunogenic properties and reduces new virions infectivity [15,16]. On the other hand, HCQ antiviral activity against COVID-19 seems to be related to its ability to modify the n-terminal glycosylation of ACE-2, leading to reduced interaction between ACE-2 and Spike and so to cell infection [8].