Controversy has surrounded the use of Hydroxychloroquine as an effective COVID-19 treatment.
Also called SARS-CoV-2, COVID-19 is similar to SARS-CoV.
That’s not my statement.
You can find that on the CDC website:
The new virus was found to be a coronavirus, and coronaviruses cause a severe acute respiratory syndrome. This new coronavirus is similar to SARS-CoV, so it was named SARS-CoV-2 The disease caused by the virus was named COVID-19 (COronVIrusDisease-2019) to show that it was discovered in 2019.
Since the COVID-19 outbreak began, there’s been an unprecedented censorship campaign against Hydroxychloroquine & Ivermectin.
There are therapeutics that knock covid out in 3 or 4 days. Yet they have banned Drs in America from prescribing HCQ and Ivermectin it’s very effective. Prevents severe illness and clears covid in a few days. Fauci let people die to push a vax that has deadly side effects
— Yolanda Goldberg (@sigstarget) October 16, 2021
In Jan 2020, MODERNA was valued at under $7 billion. Today it’s $130 billion, $120 billion increase in market capitalization. Moderna was able to obtain an Emergency Use Authorization only because they banned efficient Ivermectin & HCQ. One of the greatest scandals in history. pic.twitter.com/MdUa2ZNOQF
— Julija (@Julija9ju) October 14, 2021
We’re going to focus on Hydroxychloroquine (HCQ).
HCQ is a less toxic derivative of Chloroquine (CQ).
From Cell Discovery:
In the past years, due to infrequent utilization of CQ in clinical practice, its production and market supply was greatly reduced, at least in China. Hydroxychloroquine (HCQ) sulfate, a derivative of CQ, was first synthesized in 1946 by introducing a hydroxyl group into CQ and was demonstrated to be much less (~40%) toxic than CQ in animals4. More importantly, HCQ is still widely available to treat autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis. Since CQ and HCQ share similar chemical structures and mechanisms of acting as a weak base and immunomodulator, it is easy to conjure up the idea that HCQ may be a potent candidate to treat infection by SARS-CoV-2.
CQ & HCQ share similar chemical structures, thus it’s reasonable to hypothesize the two can treat the same illnesses.
What if I told you the NIH knew of CQ’s value for coronavirus treatment in 2005?
14 years before the discovery of SARS-CoV-2, Virology Journal released a study titled “Chloroquine is a potent inhibitor of SARS coronavirus infection and spread.”
That article is available in the NIH Library.
“2005 NIH under Fauci wrote study: Chloriquine was effective with Corona and SARS.Why did he keep quiet?”
2005 US NIH Study Found Chloroquine Was Effective in Treating Coronavirus In Primates — Why Was This Ignored? pic.twitter.com/3DEo2hUjnP
— louie (@louie82212536) April 20, 2020
Here is the direct link to 2005 NIH article touting chloriquine as a treatment for coronavirises. Oh yeah, and #BillClintonIsAPedo https://t.co/0YuqRQqYXY
— DesireePaquette (@DesireePaquette) August 4, 2020
We want treatment available. We understand that the NIH since 2005 believes Chloriquine is a potent inhibitor.
Alarming! This run on our civil liberties. Expensive invasive Medical Brown Shirts ie., Contact Tracers are being quickly organized & deployed against the citizenry.⚖ pic.twitter.com/cr0XIZwn59
— [email protected] (@TweetStreetInt1) May 9, 2020
Can anyone verify if an article by the FauXi led NIH in the Virology Journal of August 22, 2005 stating that chloriquine was *a potent inhibitor of the SARS coronavirus.” is a legitimate article?
— ✝️MAGAXMAN🇺🇸 ANGRYPATRIOT MANDATES🔄 TYRANNY (@XMANis4Real) August 23, 2021
The answer to that last question is YES.
It’s a legitimate article!
I’ve listed important findings below, but you can read the entire article at the National Center for Biotechnology Information (NCBI), a branch of the NIH:
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.
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection. In addition, the indirect immunofluorescence assay described herein represents a simple and rapid method for screening SARS-CoV antiviral compounds.
We have identified chloroquine as an effective antiviral agent for SARS-CoV in cell culture conditions, as evidenced by its inhibitory effect when the drug was added prior to infection or after the initiation and establishment of infection. The fact that chloroquine exerts an antiviral effect during pre- and post-infection conditions suggest that it is likely to have both prophylactic and therapeutic advantages. Recently, Keyaerts et al.  reported the antiviral properties of chloroquine and identified that the drug affects SARS-CoV replication in cell culture, as evidenced by quantitative RT-PCR. Taken together with the findings of Keyaerts et al. , our analysis provides further evidence that chloroquine is effective against SARS-CoV Frankfurt and Urbani strains. We have provided evidence that chloroquine is effective in preventing SARS-CoV infection in cell culture if the drug is added to the cells 24 h prior to infection. In addition, chloroquine was significantly effective even when the drug was added 3–5 h after infection, suggesting an antiviral effect even after the establishment of infection. Since similar results were obtained by NH4Cl treatment of Vero E6 cells, the underlying mechanism(s) of action of these drugs might be similar.
The NIH has known the benefits of Chloroquine to treat SARS-CoV since 2005.
Yet, it’s derivative (HCQ) suffered a smear campaign unlike anything witnessed in medical history.
Why wasn’t this study referenced at the onset of SARS-CoV-2 for the potential benefits of HCQ?
That’s something the media should ask Fauci & his NIH cronies.