>>9322973 pb

Inhibition of hepatitis C virus replication by chloroquine targeting virus-associated autophagy

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7088329/

(There's that autophagy again)

"Autophagy has been reported to play a pivotal role on the replication of various RNA viruses. In this study, we investigated the role of autophagy on hepatitis C virus (HCV) RNA replication and demonstrated anti-HCV effects of an autophagic proteolysis inhibitor, chloroquine."

(Covid 19 is an RNA virus)

"The results of this study suggest that the replication of HCV replicon utilizes machinery involving cellular autophagic proteolysis. The therapy targeted to autophagic proteolysis by using chloroquine may provide a new therapeutic option against chronic hepatitis C."

(It seems like whenever there are diseases that require autophagy to thrive, reproduce, grow, whatever, chloroquine and/or hydroxychloroquine and/or tonic water, could be helpful. When conditions - like over acid - prevent the quinine drugs from working - alkalize - like baking soda - could make the quinine drugs work better. This seems to be true with both covid 19 and cancer and maybe a whole lot of other things.

It may be true that covid 19 and cancer aren't the same thing, but if both covid 19 and cancer and other things require autophagy, and the Q drugs can stop the autophagy, the Q drugs can stop a number of different problems.)

>>9323208

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]. "