https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7199282/

Digesting the crisis: autophagy and coronaviruses

"The FDA-approved anti-malarial drugs chloroquine and hydroxychloroquine have been suggested to be repurposed for the treatment of COVID-19 [68–70], but this remains widely controversial [71–73]. Although chloroquine is a lysosomotropic agent that blocks autophagic degradation, possibly by impairing autophagosome fusion with lysosomes [74], the putative effects on autophagy may not be necessarily causal for the antiviral activity. In fact, endosomal acidification after endocytosis is critical for SARS-CoV-2 entry [75], and chloroquine inhibits this acidification [76]. In addition, chloroquine limits terminal glycosylation of the metallopeptidase ACE2, the functional receptor for SARS-CoV and SARS-CoV-2 cell entry [68, 75, 77]. Non-glycosylated ACE2 seems to interact less efficiently with the SARS-CoV spike protein, thus reducing viral entry [78]. These modes of action would target the virus upstream of autophagy, making it unlikely that autophagy modulation contributes to the outcome of chloroquine treatment at that point. Additionally, chloroquine has been shown to induce autophagy-independent effects, for instance, Golgi disorganization [74] and pulmonary vasodilation [79] that may contribute to its controversial clinical activity."

"endosomal acidification after endocytosis is critical for SARS-CoV-2 entry [75], and chloroquine inhibits this acidification [76]. "