Fauci Financial Interests versus Ethical Behavior
There has been a literal war on Hydroxychloroquine ever
since Trump began speaking highly of it. Why?
Fauci has spoken out against it, as has EVERY main stream
media outlet – Except Fox……
But why though? Well, -previous articles I have written have
given you PROOF Fauci has a financial interest in the vaccine……
Due to this fact he should NOT be advising anything
concerning Covid-19 – it is an ethical issue
When someone stands to financially profit from a vaccine
they should NOT be advising people what to do…. Let me show you WHY….
For those who do not like clicking or long reads…….
This article was published in 2005 – so the National Institute
of Health – of which Fauci is the head of – has KNOWN since 2005 (over 15
YEARS) that this medicine WORKS for SARS now has a financial interest in
selling us a vaccine rather than the medication…..
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.
So, do tell me why we have a literal cure that has been
BANNED due to Trump derangement syndrome…. Why should I be forced to take a vaccine
produced by Bill Gates who has a track record of maiming and killing children
in India and Africa with his vaccines rather than a medication with a 60 year
proven track record of being safe????
Abstract version:
Virol J. 2005; 2: 69.
Published online 2005 Aug 22. doi: 10.1186/1743-422X-2-69
PMCID: PMC1232869
PMID: 16115318
Chloroquine is a potent
inhibitor of SARS coronavirus infection and spread
Martin J Vincent,1 Eric Bergeron,2 Suzanne Benjannet,2 Bobbie R Erickson,1 Pierre E Rollin,1 Thomas G Ksiazek,1 Nabil G Seidah,2 and Stuart T Nichol1
This article has
been cited by other articles in PMC.
Abstract
Background
Severe acute
respiratory syndrome (SARS) is an emerging disease that was first reported in
Guangdong Province, China, in late 2002. The disease rapidly spread to at least
30 countries within months of its first appearance, and concerted worldwide
efforts led to the identification of the etiological agent as SARS coronavirus
(SARS-CoV), a novel member of the family Coronaviridae [1]. Complete genome sequencing of SARS-CoV [2,3] confirmed that this pathogen is not closely
related to any of the previously established coronavirus groups. Budding of the
SARS-CoV occurs in the Golgi apparatus [4] and results in the incorporation of the
envelope spike glycoprotein into the virion. The spike glycoprotein is a type I
membrane protein that facilitates viral attachment to the cellular receptor and
initiation of infection, and angiotensin-converting enzyme-2 (ACE2) has been
identified as a functional cellular receptor of SARS-CoV [5]. We have recently shown that the processing
of the spike protein was effected by furin-like convertases and that inhibition
of this cleavage by a specific inhibitor abrogated cytopathicity and significantly
reduced the virus titer of SARS-CoV [6].
Due to the
severity of SARS-CoV infection, the potential for rapid spread of the disease,
and the absence of proven effective and safe in vivo inhibitors
of the virus, it is important to identify drugs that can effectively be used to
treat or prevent potential SARS-CoV infections. Many novel therapeutic
approaches have been evaluated in laboratory studies of SARS-CoV: notable among
these approaches are those using siRNA [7], passive antibody transfer [8], DNA vaccination [9], vaccinia or parainfluenza virus expressing
the spike protein [10,11], interferons [12,13], and monoclonal antibody to the S1-subunit
of the spike glycoprotein that blocks receptor binding [14]. In this report, we describe the
identification of chloroquine as an effective pre- and post-infection antiviral
agent for SARS-CoV. Chloroquine, a 9-aminoquinoline that was identified in
1934, is a weak base that increases the pH of acidic vesicles. When added
extracellularly, the non-protonated portion of chloroquine enters the cell,
where it becomes protonated and concentrated in acidic, low-pH organelles, such
as endosomes, Golgi vesicles, and lysosomes. Chloroquine can affect virus
infection in many ways, and the antiviral effect depends in part on the extent
to which the virus utilizes endosomes for entry. Chloroquine has been widely
used to treat human diseases, such as malaria, amoebiosis, HIV, and autoimmune
diseases, without significant detrimental side effects [15]. Together with data presented here,
showing virus inhibition in cell culture by chloroquine doses compatible with
patient treatment, these features suggest that further evaluation of
chloroquine in animal models of SARS-CoV infection would be warranted as we
progress toward finding effective antivirals for prevention or treatment of the
disease.
Results
Preinfection chloroquine treatment renders
Vero E6 cells refractory to SARS-CoV infection
In order to investigate if chloroquine might prevent SARS-CoV
infection, permissive Vero E6 cells [1] were pretreated with various concentrations
of chloroquine (0.1–10 μM) for 20–24 h prior to virus infection. Cells were
then infected with SARS-CoV, and virus antigens were visualized by indirect
immunofluorescence as described in Materials and Methods. Microscopic
examination (Fig. (Fig.1A)1A) of the control cells (untreated, infected)
revealed extensive SARS-CoV-specific immunostaining of the monolayer. A
dose-dependant decrease in virus antigen-positive cells was observed starting
at 0.1 μM chloroquine, and concentrations of 10 μM completely abolished
SARS-CoV infection. For quantitative purposes, we counted the number of cells
stained positive from three random locations on a slide. The average number of
positively stained control cells was scored as 100% and was compared with the
number of positive cells observed under various chloroquine concentrations
(Fig. (Fig.1B).1B). Pretreatment with 0.1, 1, and 10 μM
chloroquine reduced infectivity by 28%, 53%, and 100%, respectively.
Reproducible results were obtained from three independent experiments. These
data demonstrated that pretreatment of Vero E6 cells with chloroquine rendered
these cells refractory to SARS-CoV infection.
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