https://newshourfirst.com/2021/01/30/440000-americans-are-dead-facebook-and-american-journal-of-medicine-admit-their-stand-on-hcq-was-wrong/?utm_campaign=shareaholic&utm_medium=reddit&utm_source=news
Note: Hydroxychloroquine and Chloroquine are not precisely the same; they are
closely related, however.
The following is what I told people nearly one year ago:
On Saturday, February 8, 2020, 09:18:29 PM PST, jim bell
<[email protected]> wrote:
[chloroquine is an old-line drug typically used against malaria]
[partial quote follows]
https://www.asbmb.org/asbmb-today/science/020620/could-an-old-malaria-drug-help-fight-the-new-coron
ASBMB Today Science Could an old malaria drug help fight the new coronavirus?
Could an old malaria drug
help fight the new coronavirus?
By John Arnst
February 06, 2020
Chloroquine might be getting new life as an antiviral treatment for the novel
coronavirus that emerged in Wuhan, China in late 2019 and has infected some
25,000 people in more than 25 countries. For decades, the drug was a front-line
treatment and prophylactic for malaria.
In a three-page paper published Tuesday in Cell Research, scientists at the
Wuhan Institute of Virology’s State Key Laboratory of Virology write that both
chloroquine and the antiviral remdesivir were, individually, “highly effective”
at inhibiting replication of the novel coronavirus in cell culture. Their drug
screen evaluated five other drugs that were not effective. The authors could
not be reached for comment.
Though the paper is brief, John Lednicky, a professor at the University of
Florida’s Emerging Pathogens Institute, found its results intriguing. “It’s
interesting in that it really lacks a lot of details but, nevertheless, if you
look at the data as presented, at least in vitro, it seems like chloroquine can
be used as an early-stage drug,” he said. “It would be very good if these types
of experiments were repeated by more laboratories to see whether the same
results occur across the board.”
Chloroquine is a synthetic form of quinine, a compound found in the bark of
cinchona trees native to Peru and used for centuries to treat malaria.
Chloroquine was an essential element of mass drug administration campaigns to
combat malaria throughout the second half of the 20th century, and remains one
of the World Health Organization’s essential medicines. However, after the
malaria parasites Plasmodium falciparum and Plasmodium vivax began exhibiting
resistance to the drug in the 1960s and 1980s, respectively, it was replaced by
similar antimalarial compounds and combination therapies. Chloroquine is still
widely used against the three other species of plasmodium and to treat
autoimmune disorders and some cases of amebiasis, an intestinal infection
caused by the amoeba Entamoeba histolytica.
Chloroquine’s antiviral properties were explored in the mid-1990s against HIV
and in the following decade against severe acute respiratory syndrome, or SARS,
which is closely related to the novel coronavirus. In 2004, researchers in
Belgium found that chloroquine inhibited replication of SARS in cell culture.
The following year, however, another team at Utah State University and the
Chinese University of Hong Kong evaluated a gamut of compounds against SARS
replication in mice infected with the virus, finding that chloroquine was only
effective as an anti-inflammatory agent. They recommended that it could be used
in combination with compounds that prevent replication. Nevertheless, in 2009,
the Belgian group found that lethal infections of human coronavirus OC43, a
relative of SARS, could be averted in newborn mice by administering chloroquine
through the mother’s milk.
[end of partial quote]
Also:
https://www.nature.com/articles/s41422-020-0282-0
Remdesivir and chloroquine effectively inhibit the recently emerged novel
coronavirus (2019-nCoV) in vitro
Manli Wang, Ruiyuan Cao, Leike Zhang, Xinglou Yang, Jia Liu, Mingyue Xu,
Zhengli Shi, Zhihong Hu, Wu Zhong & Gengfu Xiao
Cell Research (2020)Cite this article
171k Accesses
1108 Altmetric
Metrics
details
Dear Editor,
In December 2019, a novel pneumonia caused by a previously unknown pathogen
emerged in Wuhan, a city of 11 million people in central China. The initial
cases were linked to exposures in a seafood market in Wuhan.1 As of January 27,
2020, the Chinese authorities reported 2835 confirmed cases in mainland China,
including 81 deaths. Additionally, 19 confirmed cases were identified in Hong
Kong, Macao and Taiwan, and 39 imported cases were identified in Thailand,
Japan, South Korea, United States, Vietnam, Singapore, Nepal, France, Australia
and Canada. The pathogen was soon identified as a novel coronavirus
(2019-nCoV), which is closely related to sever acute respiratory syndrome CoV
(SARS-CoV).2 Currently, there is no specific treatment against the new virus.
Therefore, identifying effective antiviral agents to combat the disease is
urgently needed.
An efficient approach to drug discovery is to test whether the existing
antiviral drugs are effective in treating related viral infections. The
2019-nCoV belongs to Betacoronavirus which also contains SARS-CoV and Middle
East respiratory syndrome CoV (MERS-CoV). Several drugs, such as ribavirin,
interferon, lopinavir-ritonavir, corticosteroids, have been used in patients
with SARS or MERS, although the efficacy of some drugs remains controversial.3
In this study, we evaluated the antiviral efficiency of five FAD-approved drugs
including ribavirin, penciclovir, nitazoxanide, nafamostat, chloroquine and two
well-known broad-spectrum antiviral drugs remdesivir (GS-5734) and favipiravir
(T-705) against a clinical isolate of 2019-nCoV in vitro.
Standard assays were carried out to measure the effects of these compounds on
the cytotoxicity, virus yield and infection rates of 2019-nCoVs. Firstly, the
cytotoxicity of the candidate compounds in Vero E6 cells (ATCC-1586) was
determined by the CCK8 assay. Then, Vero E6 cells were infected with
nCoV-2019BetaCoV/Wuhan/WIV04/20192 at a multiplicity of infection (MOI) of 0.05
in the presence of varying concentrations of the test drugs. DMSO was used in
the controls. Efficacies were evaluated by quantification of viral copy numbers
in the cell supernatant via quantitative real-time RT-PCR (qRT-PCR) and
confirmed with visualization of virus nucleoprotein (NP) expression through
immunofluorescence microscopy at 48 h post infection (p.i.) (cytopathic effect
was not obvious at this time point of infection). Among the seven tested drugs,
high concentrations of three nucleoside analogs including ribavirin
(half-maximal effective concentration (EC50) = 109.50 μM, half-cytotoxic
concentration (CC50) > 400 μM, selectivity index (SI) > 3.65), penciclovir
(EC50 = 95.96 μM, CC50 > 400 μM, SI > 4.17) and favipiravir (EC50 = 61.88 μM,
CC50 > 400 μM, SI > 6.46) were required to reduce the viral infection (Fig. 1a
and Supplementary information, Fig. S1). However, favipiravir has been shown to
be 100% effective in protecting mice against Ebola virus challenge, although
its EC50 value in Vero E6 cells was as high as 67 μM,4 suggesting further in
vivo studies are recommended to evaluate this antiviral nucleoside. Nafamostat,
a potent inhibitor of MERS-CoV, which prevents membrane fusion, was inhibitive
against the 2019-nCoV infection (EC50 = 22.50 μM, CC50 > 100 μM, SI > 4.44).
Nitazoxanide, a commercial antiprotozoal agent with an antiviral potential
against a broad range of viruses including human and animal coronaviruses,
inhibited the 2019-nCoV at a low-micromolar concentration (EC50 = 2.12 μM; CC50
> 35.53 μM; SI > 16.76). Further in vivo evaluation of this drug against
2019-nCoV infection is recommended. Notably, two compounds remdesivir (EC50 =
0.77 μM; CC50 > 100 μM; SI > 129.87) and chloroquine (EC50 = 1.13 μM; CC50 >
100 μM, SI > 88.50) potently blocked virus infection at low-micromolar
concentration and showed high SI (Fig. 1a, b).
