There was, actually, a 2005 study listed in the NIH National Library of Medicine (yes, Director Fauci’s NIH) literature that showed Chloroquine/HCQ effective against Sars Cov 2.
Chloroquine is a Potent Inhibitor of SARS Coronavirus Infection and Spread
Martin J Vincent et al. Virol J. 2005.
Abstract
Background: Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results: 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.
Conclusion: 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.
The differences between chloroquine and hydroxychloroquine are outlined in an article below. Basically, hydroxychloroquine was synthesized in 1946 as a safer alternative to chloroquine. Also published by Pubmed an NIH National Library of Medicine. 2014
The 4-aminoquinolines are weak bases that are completely absorbed from the gastrointestinal tract, sequestered in peripheral tissues, metabolized in the liver to pharmacologically active by-products, and excreted via the kidneys and the feces. The parent drugs and metabolites are excreted with a half-life of elimination of approximately 40 days. However, slow release from sequestered stores of the drugs means that after discontinuation, they continue to be released into the plasma for years. Correct dosing is based on the ideal body weight of the patient, which depends on height. The 4AQs diminish autoimmunity without compromising immunity to infections.
Keywords: Rheumatoid Arthritis, Systemic Lupus Erythematosus, Blood Concentration, Ideal Body Weight, Therapeutic Ratio
This chapter covers the pharmacology of chloroquine and hydroxychloroquine, which is similar for both drugs [1], but the details are different. For example, both drugs are partially excreted in feces, but the proportions differ slightly—8–10 % for chloroquine and 15–24 % for hydroxychloroquine. Generally, whatever is said in this chapter about one drug can be assumed to apply to the other unless otherwise specified [1, 2]. Because both drugs are derivatives of a 4-aminoquinoline (4AQ) nucleus, they are referred to as 4AQs, and the retinopathy that they can cause is termed 4-aminoquinoline retinopathy (4AQR) [3]. Commonly used abbreviations in this chapter are collected in “Abbreviations” for reference. Each term will be first used in its full form, along with its abbreviation.
History
In the 1600s, the Jesuits who proselytized Chile discovered from the Incas that the bark of the cinchona tree can cure malaria [4, 5]. Additional medicinal qualities of cinchona bark were described in the 1700s, and the British and Dutch transplanted these trees to Javan plantations in the early 1900s for the production of quinine. In 1894, Payne described the use of quinine to treat systemic lupus erythematosus (SLE) [6]. Other alkaloids contained in cinchona bark, such as pamaquine, were also successfully used to treat SLE [5].
When the Japanese army occupied Java in World War II, the natural supply of quinine was lost, and synthesis of antimalarials was pursued in the United States [7]. Quinacrine, a 9-aminoacridine compound, was first used, but had the unpleasant side effect of staining the skin and sclera yellow in a manner indistinguishable from icterus [8–10]. The 4AQs, chloroquine and hydroxychloroquine, were found to be effective as antimalarials and did not discolor the skin. Chloroquine was first synthesized in 1934 by Andersag of I.G. Farbenindustrie in a German effort to find drugs better than quinine [11]. The Germans lost interest in the drug when they judged it to be too toxic for use in man, but the Americans restudied the drug and found it to be effective against malaria and sufficiently safe [3, 7, 12]. Hydroxychloroquine was synthesized in 1946 and proposed as a safer alternative to chloroquine in 1955 [13]. Resistance to chloroquine as an antimalarial became a problem in some parts of the world in the 1980s.
In World War II it was observed that servicemen with rashes and inflammatory arthritis who took quinacrine and chloroquine for malaria prophylaxis experienced improvement in their autoimmune conditions [14]. In 1951, Page used quinacrine to treat arthritis and autoimmune dermatologic conditions [15]. Later chloroquine and then hydroxychloroquine were also noted to favorably affect patients with rheumatologic diseases. Over time, both have been widely adopted for these uses. They are commonly used in patients with rheumatoid arthritis (RA), SLE, discoid lupus erythematosus, polymorphous light eruptions, solar urticaria, recurrent basal cell carcinoma of the skin, porphyrea cutane tarda, antiphospholipid antibody syndrome, and more than 20 other rarer conditions [11, 16–20].
Best synopsis I have seen. Kudos, Michael.
There was, actually, a 2005 study listed in the NIH National Library of Medicine (yes, Director Fauci’s NIH) literature that showed Chloroquine/HCQ effective against Sars Cov 2.
Chloroquine is a Potent Inhibitor of SARS Coronavirus Infection and Spread
Martin J Vincent et al. Virol J. 2005.
Abstract
Background: Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results: 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.
Conclusion: 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.
Full:
https://pubmed.ncbi.nlm.nih.gov/16115318/
The differences between chloroquine and hydroxychloroquine are outlined in an article below. Basically, hydroxychloroquine was synthesized in 1946 as a safer alternative to chloroquine. Also published by Pubmed an NIH National Library of Medicine. 2014
2014 Apr 4 : 35–63. Published online 2014 Apr 4. doi: 10.1007/978-1-4939-0597-3_2
PMCID: PMC7122276 | David J. Browning corresponding author2
Pharmacology of Chloroquine and Hydroxychloroquine
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7122276/
Abstract
The 4-aminoquinolines are weak bases that are completely absorbed from the gastrointestinal tract, sequestered in peripheral tissues, metabolized in the liver to pharmacologically active by-products, and excreted via the kidneys and the feces. The parent drugs and metabolites are excreted with a half-life of elimination of approximately 40 days. However, slow release from sequestered stores of the drugs means that after discontinuation, they continue to be released into the plasma for years. Correct dosing is based on the ideal body weight of the patient, which depends on height. The 4AQs diminish autoimmunity without compromising immunity to infections.
Keywords: Rheumatoid Arthritis, Systemic Lupus Erythematosus, Blood Concentration, Ideal Body Weight, Therapeutic Ratio
This chapter covers the pharmacology of chloroquine and hydroxychloroquine, which is similar for both drugs [1], but the details are different. For example, both drugs are partially excreted in feces, but the proportions differ slightly—8–10 % for chloroquine and 15–24 % for hydroxychloroquine. Generally, whatever is said in this chapter about one drug can be assumed to apply to the other unless otherwise specified [1, 2]. Because both drugs are derivatives of a 4-aminoquinoline (4AQ) nucleus, they are referred to as 4AQs, and the retinopathy that they can cause is termed 4-aminoquinoline retinopathy (4AQR) [3]. Commonly used abbreviations in this chapter are collected in “Abbreviations” for reference. Each term will be first used in its full form, along with its abbreviation.
History
In the 1600s, the Jesuits who proselytized Chile discovered from the Incas that the bark of the cinchona tree can cure malaria [4, 5]. Additional medicinal qualities of cinchona bark were described in the 1700s, and the British and Dutch transplanted these trees to Javan plantations in the early 1900s for the production of quinine. In 1894, Payne described the use of quinine to treat systemic lupus erythematosus (SLE) [6]. Other alkaloids contained in cinchona bark, such as pamaquine, were also successfully used to treat SLE [5].
When the Japanese army occupied Java in World War II, the natural supply of quinine was lost, and synthesis of antimalarials was pursued in the United States [7]. Quinacrine, a 9-aminoacridine compound, was first used, but had the unpleasant side effect of staining the skin and sclera yellow in a manner indistinguishable from icterus [8–10]. The 4AQs, chloroquine and hydroxychloroquine, were found to be effective as antimalarials and did not discolor the skin. Chloroquine was first synthesized in 1934 by Andersag of I.G. Farbenindustrie in a German effort to find drugs better than quinine [11]. The Germans lost interest in the drug when they judged it to be too toxic for use in man, but the Americans restudied the drug and found it to be effective against malaria and sufficiently safe [3, 7, 12]. Hydroxychloroquine was synthesized in 1946 and proposed as a safer alternative to chloroquine in 1955 [13]. Resistance to chloroquine as an antimalarial became a problem in some parts of the world in the 1980s.
In World War II it was observed that servicemen with rashes and inflammatory arthritis who took quinacrine and chloroquine for malaria prophylaxis experienced improvement in their autoimmune conditions [14]. In 1951, Page used quinacrine to treat arthritis and autoimmune dermatologic conditions [15]. Later chloroquine and then hydroxychloroquine were also noted to favorably affect patients with rheumatologic diseases. Over time, both have been widely adopted for these uses. They are commonly used in patients with rheumatoid arthritis (RA), SLE, discoid lupus erythematosus, polymorphous light eruptions, solar urticaria, recurrent basal cell carcinoma of the skin, porphyrea cutane tarda, antiphospholipid antibody syndrome, and more than 20 other rarer conditions [11, 16–20].