Published August 22, 2005, in the Virology Journal Chloroquine is a potent inhibitor of SARS coronavirus infection and spread Martin J Vincent et al. Excerpts in italics with my bolds.
The lead author worked at Special Pathogens Branch, Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, Georgia, 30333, USA. Virology Journal is a publication of the National Institutes of Health, which Anthony Fauci joined in 1968 and since 1984 he has directed the National Institute of Allergy and Infectious Diseases. (NIAID).
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
The infectivity of coronaviruses other than SARS-CoV are also affected by chloroquine, as exemplified by the human CoV-229E . The inhibitory effects observed on SARS-CoV infectivity and cell spread occurred in the presence of 1–10 μM chloroquine, which are plasma concentrations achievable during the prophylaxis and treatment of malaria (varying from 1.6–12.5 μM)  and hence are well tolerated by patients. It recently was speculated that chloroquine might be effective against SARS and the authors suggested that this compound might block the production of TNFα, IL6, or IFNγ . Our data provide evidence for the possibility of using the well-established drug chloroquine in the clinical management of SARS.
Chloroquine, a relatively safe, effective and cheap drug used for treating many human diseases including malaria, amoebiosis and human immunodeficiency virus is effective in inhibiting the infection and spread of SARS CoV in cell culture. The fact that the drug has significant inhibitory antiviral effect when the susceptible cells were treated either prior to or after infection suggests a possible prophylactic and therapeutic use.
This means, of course, that Dr. Fauci has known for 15 years that chloroquine and it’s even milder derivative hydroxychloroquine (HCQ) will not only treat a current case of coronavirus (“therapeutic”) but prevent future cases (“prophylactic”). So HCQ functions as both a cure and a vaccine. In other words, it’s a wonder drug for coronavirus. Said Dr. Fauci’s NIH in 2005, “concentrations of 10 μM completely abolished SARS-CoV infection.” Fauci’s researchers add, “chloroquine can effectively reduce the establishment of infection and spread of SARS-CoV.”
In connection with the SARS outbreak – caused by a coronavirus dubbed SARS- CoV – the NIH researched chloroquine and concluded that it was effective at stopping the SARS coronavirus in its tracks. The COVID-19 bug is likewise a coronavirus, labeled SARS-CoV-2. While not exactly the same virus as SARS-CoV-1, it is genetically related to it, and shares 79% of its genome, as the name SARS-CoV-2 implies. They both use the same host cell receptor, which is what viruses use to gain entry to the cell and infect the victim.
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