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Author Topic: COVID-19 🏴☠️ Pandemic  (Read 15752 times)

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AGelbert

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May 1,2020  US COVID-19 Total Cases 😷 PASSES ONE MILLION 😖
Click on image below for update:

Agelbert NOTE: This is the American (Medical Industrial Complex = EXPENSIVE instead of nearly free as in Cuba) version of the Drug Cuba has been using successfully to treat COVID-19 patients:

Interferon alfa-2b

US: C (Risk not ruled out)
Routes of administration   Subcutaneous, intramuscular
ATC code   
L03AB05 (WHO)
Legal status
Legal status   
UK: POM (Prescription only)
US: ℞-only
Identifiers
IUPHAR/BPS   
8338
DrugBank   
DB00105 ☒
ChemSpider   
none
ChEMBL   
ChEMBL1201558 ☒

Interferon alfa-2b is an antiviral or antineoplastic drug. It is a recombinant form of the protein Interferon alpha-2 that was originally sequenced and produced recombinantly in E. coli[1] in the laboratory of Charles Weissmann at the University of Zurich, in 1980.[2][3] It was developed at Biogen, and ultimately marketed by Schering-Plough under the trade name Intron-A. It was also produced in 1986 in recombinant human form, in the Center for Genetic Engineering and Biotechnology of Havana, Cuba, under the name Heberon® Alfa R[4].

It has been used for a wide range of indications, including viral infections and cancers. This drug is approved around the world for the treatment of chronic hepatitis C, chronic hepatitis B, hairy cell leukemia, Behçet's disease, chronic myelogenous leukemia, multiple myeloma, follicular lymphoma, carcinoid tumor, mastocytosis and malignant melanoma.

The medication is being used in clinical trials to treat patients with SARS-CoV-2[5] although there are no yet published results of those trials on peer-reviewed scientific literature.

So far, two non-peer reviewed research articles have been published. One study at the University of Texas Medical Branch, Galveston, showed evidence of a direct anti-viral effect of Interferon alpha against novel Coronavirus in vitro. The study demonstrated around 10,000 fold reduction in the quantity of virus that was pre-treated with Interferon alpha 48 hours earlier. A second study by universities in China, Australia and Canada analysed 77 moderate COVID-19 subjects in Wuhan and observed that those who received Interferon alpha-2b showed a significant reduction in the duration of virus shedding period and even in levels of the inflammatory cytokine, IL-6. [6] [7]
https://en.wikipedia.org/wiki/Interferon_alfa-2b
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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System Update with Glenn Greenwald - The Three-Pronged Crisis Imperiling the Bolsonaro Government
9,956 views•Premiered Apr 30, 2020


The Intercept
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In the fifth episode of The Intercept's weekly show, host Glenn Greenwald does a deep dive on the combined crisis of coronavirus, economic upheaval and a grave corruption scandal that is shaking Brazil. Watch as Glenn ties together the different sides of this crisis, and how it is affecting the biggest country in South America.


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Category News & Politics
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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Domestic Workers Struggle to Make Ends Meet During COVID-19 | NowThis
6,743 views•May 1, 2020


NowThis News
696K subscribers

‘I can’t even sleep at night to figure out which bills to pay or not pay.’ — America’s 2.5 million domestic workers are facing unprecedented financial and health risks to make ends meet during COVID-19.
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In US news and current events today, these domestic workers face dangerous financial & health risks as they struggle to make ends meet amid the pandemic. Watch this video to learn about the obstacles Covid-19 is creating for domestic workers and learn how to better support them.

For the latest coronavirus news and COVID-19 updates, subscribe to NowThis News.

Quote
Human Inequity is directly proportional to the amount of human iniquity. - A. G. Gelbert
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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Trump Administration Spreading The Pandemic With Air Deportation Flights
By Dan Beeton, CEPR.net. Washington, DC  ―  New analysis from the Center for Economic and Policy Research (CEPR) shows that Immigrations and Customs Enforcement (ICE) likely has carried out at least 232 deportation flights to Latin American and Caribbean countries since February 3, 2020, just after the Trump administration declared a public health emergency due to the COVID-19 pandemic. By examining flight data for known ICE Air contractors taking off from airports near ICE detention facilities, with destinations frequently used for deportations, CEPR is able to provide estimates of the numbers of... - more -
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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May 2,2020 🏴 COVID-19 MAY 2, 2020 🏴 GLOBAL DEATHS EXCEED 2017 ANNUAL PROTEIN-ENERGY MALNUTRITON DEATHS ☠️

Agelbert NOTE:   COVID-19 has already caused more deaths per year, compared to 2017, from the greatest to the least, than Maternal Disorders, Alcohol Use Disorders, Drug Use Disorders, Conflict, Hepatitis, Fire, Poisonings, Heat (hot and cold exposure), Terrorism and Natural Disasters. Remember that when you are told by the politicians from both wings of the 💵😈🎩 Capitalists 'R' US DUOPOLY that the 🦍 MIC Pentagon MASSIVE BUDGET SWAG off we-the-people's dime is "justified".
Click on image below for update:

Agelbert NOTE: This is the American (Medical Industrial Complex = EXPENSIVE instead of nearly free as in Cuba) version of the Drug Cuba has been using successfully to treat COVID-19 patients:

Interferon alfa-2b

US: C (Risk not ruled out)
Routes of administration   Subcutaneous, intramuscular
Legal status UK: POM (Prescription only) US: ℞-only
Identifiers IUPHAR/BPS   

Interferon alfa-2b is an antiviral or antineoplastic drug. It is a recombinant form of the protein Interferon alpha-2 that was originally sequenced and produced recombinantly in E. coli[1] in the laboratory of Charles Weissmann at the University of Zurich, in 1980.[2][3] It was developed at Biogen, and ultimately marketed by Schering-Plough under the trade name Intron-A. It was also produced in 1986 in recombinant human form, in the Center for Genetic Engineering and Biotechnology of Havana, Cuba, under the name Heberon® Alfa R[4].

It has been used for a wide range of indications, including viral infections and cancers. This drug is approved around the world for the treatment of chronic hepatitis C, chronic hepatitis B, hairy cell leukemia, Behçet's disease, chronic myelogenous leukemia, multiple myeloma, follicular lymphoma, carcinoid tumor, mastocytosis and malignant melanoma.

The medication is being used in clinical trials to treat patients with SARS-CoV-2[5] although there are no yet published results of those trials on peer-reviewed scientific literature.

So far, two non-peer reviewed research articles have been published. One study at the University of Texas Medical Branch, Galveston, showed evidence of a direct anti-viral effect of Interferon alpha against novel Coronavirus in vitro. The study demonstrated around 10,000 fold reduction in the quantity of virus that was pre-treated with Interferon alpha 48 hours earlier. A second study by universities in China, Australia and Canada analysed 77 moderate COVID-19 subjects in Wuhan and observed that those who received Interferon alpha-2b showed a significant reduction in the duration of virus shedding period and even in levels of the inflammatory cytokine, IL-6. [6] [7]
https://en.wikipedia.org/wiki/Interferon_alfa-2b
« Last Edit: May 04, 2020, 11:29:55 am by AGelbert »
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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New York Gov. Cuomo Delivers COVID-19 Update | LIVE | NowThis
19,822 views•Streamed live 11 hours ago


NowThis News
699K subscribers

HAPPENING NOW—CUOMO UPDATE: New York Gov. Andrew Cuomo is at an MTA facility in Flushing, Queens, where he will deliver an update on the state’s response to the coronavirus outbreak. This week, he announced that the NYC subway would be suspending service from 1 am-5 am everyday so that the trains can be cleaned and disinfected. Cuomo called the move ‘as ambitious as anything we’ve ever undertaken.’ This comes as many people experiencing homelessness across NYC have turned to the subway to be a safe place to go during the pandemic, as they fear the coronavirus would spread more rapidly within homeless shelters.

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#AndrewCuomo #Coronavirus #NewYork #News #NowThis #NowThisNews
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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Re: COVID-19 🏴☠️ Pandemic
« Reply #246 on: May 03, 2020, 01:11:57 pm »


May 3,2020 COVID-19

Agelbert NOTE:   COVID-19 has already caused more deaths per year, compared to 2017, from the greatest to the least, than Maternal Disorders, Alcohol Use Disorders, Drug Use Disorders, Conflict, Hepatitis, Fire, Poisonings, Heat (hot and cold exposure), Terrorism and Natural Disasters. Remember that when you are told by the politicians from both wings of the 💵😈🎩 Capitalists 'R' US DUOPOLY that the 🦍 MIC Pentagon MASSIVE BUDGET SWAG off we-the-people's dime is "justified".
Click on image below for update:

« Last Edit: May 03, 2020, 09:03:39 pm by AGelbert »
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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Doctors Face Troubling Question: Are They Treating Coronavirus Correctly?


More video:

ANOTHER WHISTLEBLOWER NURSE
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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May 4,2020 COVID-19 🚩 Florida 🤢 Hospitalizations Rising Rapidly

Click on image below for update:


Science Behind Covid 19 Being Man Made


176 watching now•Started streaming 17 minutes ago

Jamarl Thomas
28K subscribers

Support the stream: https://streamlabs.com/jamarlthomas

Nina Turner Flirts With Third Party, Jessie Ventura 2020 Run, Science Behind Covid 19 Being Man Made

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#Bernie2020 #NeverBiden #dropoutjoe

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Category News & Politics
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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COVID-19: Questionable Coronavirus Evolution in Biosafety Level 4 Labs

By 👩‍⚕️ Dady Chery ✨

Agelbert NOTE: Dr. Dady Chery is an Associate Professor of Biology. She is a scientist that knows what Viruses DO and HOW they DO IT. She is no "conspiracy theorist". She is a hard nosed scientist that sees through any pseudo-scientific happy talk and has the courage to challenge Medical Industrial Complex mendacity. It would be prudent, considering the danger to human health from the SARS-CoV-2 virus that kills so many people through COVID-19, for all of us to to take her 📢 whistleblowing revelations and warnings seriously.

May 1, 2020 at 9:25 am


In one of the greatest scientific understatements since Watson and Crick wrote, “it has not escaped our notice…” in their famous 1953 paper on the double-helical structure of DNA, the authors of a January 2020 paper concluded: “our findings suggest unconventional evolution of 2019-nCoV that warrants further investigation.” The authors of the more recent paper have been forced to withdraw it, but Dr. Luc Montagnier, who is not one to shirk from a fight and won the Nobel Prize in 2008 for his discovery of the means to culture HIV, has kept their story alive by publicly defending the results. The article is available online, apparently so it may be attacked. Briefly, it shows that, compared to the 2002 SARS-CoV, and in fact the entire Coronaviridae family, the agent of COVID-19 contains, in its surface spike protein, several small regions that are related to HIV. The probability that this could have happened by chance or through any known natural process is essentially zero.


The lead author on that paper, Dr. Prashant Pradhan, is sufficiently expert in such analyses that he has developed his own program, called the MEGAX Software, for building phylogenetic trees. Nevertheless, he is treated in the assaults on his paper as if he were a neophyte. When he did this study 55 coronavirus sequences were available, including 27 clinical SARS-CoV-2 isolates. There was also the sequence of a virus that had supposedly been collected in 2013 from a bat in Yunnan (BETACOV/BAT/YUNNAN/RATG13/2013/EPI_ISL_402131). Curiously, the Wuhan Institute of Virology entered the information about that bat virus, also called RaTG13, into the sequence database seven years late: in January 2020. The bat virus turned out to resemble SARS-CoV-2 more than any other virus, but exclusively in one protein: the surface spike! As for the rest, the bat virus was obviously a beta-coronavirus, but one evolutionarily quite different from SARS-CoV-2. A reasonable analogy for this bat virus and its fortuitous spike protein sequence would be to dig up, for a comparison to humans, a chimpanzee that had a perfectly human head but was a chimpanzee in every other detail. An unconventional evolution: to say the least.


A notable difference between SARS-CoV-2 and other coronaviruses was several tiny insertions in the spike protein, which accounted altogether for about two percent of the whole protein. More precisely, there were four insertions in all, each one with six to eight contiguous residues, in a protein with a total of about 1,280 residues. Imagine a chain that should have 1,280 green beads, but four clusters of six to eight red beds are in it at different places. The points of insertion looked exactly like the kinds of places where a simple-minded student would have put them. They were located in the protein where one might naively guess that some variation might be tolerated, and where the inserts might wind up being presented on the protein surface.


Now, suppose there were 20 different shades of red to pick from, like there are 20 different kinds of residues in proteins. The probability of finding by chance a specific sequence of seven different shades, or consecutive protein residues, is roughly 8 in 10 billion, and the probability of finding three such sequences in a protein with only 1,280 residues is essentially zero. Nevertheless, all four inserts are in the SARS-CoV-2 spike protein; furthermore, they correspond to HIV sequences. In my view, the first three are most convincing, and they all correspond to parts of an HIV protein called GP120. This does not happen by chance either.

GP120 is to HIV as the spike protein is to coronaviruses. Just like SARS-CoV-2 uses the spike protein to recognize the human ACE2 protein on lung epithelial cells for example, HIV uses its GP120 protein to recognize the human CD4 protein on a subset of white blood cells called CD4 T-lymphocytes. The reason HIV infections are so devastating is because the virus attacks the very cells that would trigger the body’s response to an infection. More than 80 percent of hospitalized COVID-19 patients show a substantial drop in their blood lymphocytes: a condition called lymphocytopenia. This condition is probably unrelated to the HIV sequences in SARS-CoV-2, however, because it was also present in SARS-CoV. So the HIV sequences in SARS-CoV-2 did not work.


I am a scientist, and as a rule, I do not subscribe to conspiracy theories. This is partly because I believe that such theories are an intellectually lazy way to substitute another power for the traditional Abrahamic deity. I am also convinced that natural selection can generate more diversity in living things, including viruses, than any other process and can sometimes find painful ways to punish, or even extinguish, species that take more than their share of resources. Finally, I do not believe that governments or their agencies are sufficiently smart to concoct all the schemes ascribed to them. Though they can behave maliciously, the most terrible things they do are usually the results of inaction and stupidity.

Might a group of scientists have created a virus that could potentially attack human T-lymphocytes as well as human lung epithelial cells? I have sadly come to conclude that the short answer to this question is “yes.” I have looked more closely at the Wuhan facilities and the kind of research routinely done there, and the following is a glimpse of what I found.


The laboratories in Wuhan began modestly enough in 1956 as an agricultural microbiology facility. This facility has, however, gradually acquired Biosafety Level 2 and 3 (BSL-2, BSL-3) laboratories in which to work on potentially harmful microbes. After the SARS-CoV epidemic of 2002, and the H5N1 avian flu of 2003, France and China collaborated to create a $42.4 million Biosafety Level 4 (BSL-4, or P4) laboratory. This is the highest level of safety for biological research, and there exist only about 30 such laboratories. They are designed for work on lethal human pathogens, including viruses like the Ebola, Zika, and coronaviruses, for which there is no vaccine. The BSL-4 Wuhan facility was modeled on the Jean Mérieux-INSERM Laboratory in Lyon, France.


From the start, the research in Wuhan has been highly collaborative and international. The Wuhan Institute of Virology boasts of partnerships with organizations that include the European Union, the United Nations Food and Agriculture Organization (FAO), and the United Nations World Health Organization (WHO); and countries that include, not only France, but also the United States, Canada, the United Kingdom, Australia, Spain, Germany, the Netherlands, Japan, Singapore, Pakistan, Islamabad, and Kenya. Scientists from other BSL-4 laboratories, like those in France, at Australia’s Animal Health Laboratory, and the Galveston National Laboratory of the University of Texas, cross-train each other’s students and rotate through Wuhan. Theirs is a chummy and exclusive club that works outside the scrutiny of most scientists. Their results cannot be verified without access to BSL-4 facilities, which is granted to few.


As an example of work that was done in collaboration with Wuhan, I offer a 2015 paper on coronaviruses that caused some controversy because it involved the creation of a human pathogen from a harmless virus. This research involved scientists at the University of North Carolina at Chapel Hill, the National Center for Toxicological Research of the Food and Drug administration in Arkansas, the Key Laboratory of Special Pathogens and Biosafety at the Wuhan Institute of Virology, the Institute for Research in Biomedicine at the Bellinzona Institute of Microbiology in Zurich, and the Harvard Medical School. Support for the work came mainly from National Institutes of Allergy and Infectious Diseases (NIAID) funds to the US researchers, National Natural Science Foundation of China funds to the Wuhan researchers, and, curiously, money from USAID-EPT-PREDICT EcoHealth Alliance to a Wuhan researcher. That researcher was Shi Zhengli, the Director of the Wuhan Institute of Virology, better known as China’s Batwoman. The benign sounding EcoHealth Alliance finances the collection of pathogens from animals and humans throughout the world. I chose this particular example because, in my view, it involved the same skill set and vacuity as the kind of research that put the HIV inserts in SARS-CoV-2.


The 2015 study began with an innocuous horseshoe-bat coronavirus, called RsSHC014-CoV, which could not harm mice, or infect human lung cells in test tubes in the lab, but could infect monkey cells in test tubes. The researchers then excised the spike-protein region from a SARS-CoV virus (that had been altered to infect mice) and substituted in its stead the spike-protein region from RsSHC014-CoV. The resulting chimera turned out to cause rapid weight loss in mice. Furthermore, the chimeric virus could infect human lung cells in test tubes and was probably pathogenic on humans. The reason the chimeric virus could infect human lung cells turned out to be because it had gained the ability to recognize the human ACE2 protein on the cells.


The researchers tried, by various approaches, to neutralize the little monster they had created. They tested several antibodies they had on hand against SARS-CoV to see if they would also work against the chimeric virus, but the antibodies worked poorly or not at all in preventing infections by the new virus. They attempted to vaccinate mice with the killed virus. These vaccinations not only failed but also were actually harmful to the mice. In particular, they suffered lung damage when they were subsequently exposed to the virus, whereas the unvaccinated mice did not. The researchers also tried to do vaccinations with live virus, but such vaccinations required so much virus that they could be done only on the young mice that needed them least, and would have killed the aged mice, which were the population that most required protection. Though there is a lesson to be learned here about the potential dangers of vaccination against coronaviruses, this research was hardly worth the risk of a possible pandemic by an escaped man-made virus.


The flow chart for the above research is quite characteristic of the kind of work that gets done in BSL-4 labs. It may be summarized as follows:

• Find a nasty pathogen in nature, or create one by a bit of ordinary cloning.

• Test the pathogen’s ability to grow in vitro on various mammalian cells.

• Test the pathogen’s ability to cause illness in or death of live mammals, like mice.

• Try to figure out, from a number of well-established receptor proteins identified by legitimate laboratories, which human protein the pathogen might recognize.

• Try to neutralize the pathogen with antibodies in vitro.

• Check if the killed pathogen or a low number of the live pathogen will work as a vaccine in live mammals, like mice, and protect them in future encounters with the pathogen.



This is the identical flow chart that is probably followed for the development of bioweapons. In particular, if a vaccine can be raised against a pathogen, then this allows its creator to vaccinate himself and safely use the pathogen as a weapon against his imagined enemies. It is a banally evil path that is well trod by a particular kind of pedestrian scientist.


The sort of study where a scientist creates a pathogen is politely labeled gain-of-function research by biologists. It raises eyebrows in the scientific community whenever such work gets generously funded or prominently published, like the paper I just described, which appeared in the journal Nature Medicine in 2015. Gain-of-function research continues to be funded, however, with no oversight from the public that finances it and is most likely to suffer from it. For the most part, this kind of research goes unpublished. It has been suggested, for example, that the insertion of HIV sequences in SARS-CoV-2 might have been a foolhardy attempt to create a virus for vaccination against HIV.


The lead researchers of the 2015 research continue their work. In fact, one recently tried to put a coronavirus in a fruit bat. Another collaborates with the for-profit pharmaceutical company, Gilead Sciences, in development of drugs against coronaviruses, even as he enjoys millions of taxpayer dollars for his research, mostly via the NIAID. Dr. Anthony Fauci has directed the NIAID since 1984. He also promotes Gilead. During his tenure at NIAID, the federal committees that weigh the risks and benefits of gain-of-function research have been anonymous, closed-door, and without citizen oversight. Consider for a moment the sobering fact that, if SARS-CoV-2, an airborne virus, had efficiently recognized CD4 T-lymphocytes with its HIV sequences, the death toll from COVID-19 might now be millions instead of hundreds of thousands of people. The sacrifice of even one person for such worthless and repugnant research is too much. The COVID-19 pandemic offers an occasion to make urgent changes in science policy.


Editor’s Notes: Dr. Dady Chery is an Associate Professor of Biology, Co-Editor-In-Chief of News Junkie Post, and the author of We Have Dared to Be Free: Haiti’s Struggle Against Occupation. Photographs one, two, five, eight, eleven and twelve from the archive of Prachatai; photograph three and fourteen from the archive of The National Institute of Health; composite six from the archive of Jun Frogosa; photograph nine by Chad Davis; photograph ten from the archive of Shantanu Dutta; and photographs seven,thirteen and fifteen by Jon Roman.

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August 28, 2014 Ebola: Zombie Apocalypse, Biological Warfare or Marketing Hype?
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http://newsjunkiepost.com/2020/05/01/covid-19-questionable-coronavirus-evolution-in-biosafety-level-4-labs/

Agelbert Public Service NOTE: ACE2 is an acronym for Angiotensin-converting enzyme 2. "Enzyme" is another word for "Catalyst". An enzyme is a substance, usually a protein, that promotes a chemical reaction in which the enzyme itself is not changed. The role of enzymes in the human body is to inititate chemical reactions at a lower temperature than would normally be required to do so AND modulate the reactions by keeping them from raising your body temperature to a tissue killing level. That's what our life preserving biochemical homoestatic control of body temperature within a certain band is all about. IOW, they modulate the reaction they promote so that it goes at a slower than "normal" (i.e. if no enzyme/catalyst had started and mediated the chemcal reaction) rate.

The ACE2 receptors on lung cells (and heart, kidney, intestines and arterial blood vessel smooth muscle endothelial cells) convert a vasoconstricting enzyme (i.e. an enzyme that raises your blood pressure by constricting the places where your blood flows) to a blood pressure lowering, vasodilating enzyme (i.e. an enzyme that expands the places where your blood flows by relaxing the smooth muscles in them).

When SARS-CoV-2 blocks the ACE2 receptor, you have a higher risk of damage from high blood pressure, in addition to the severe impairment of your lung cells' ability to replace excess carbon dioxide with sufficient oxygen to keep all your tissues functioning properly. That's the Cliffs Notes version of the situation. SARS-CoV-2 gains entry into cells through the ACE2 Receptor, at which time it proceeds to hijack the cell machinery to replicate.
« Last Edit: May 04, 2020, 05:04:00 pm by AGelbert »
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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Could Retroviruses Play a Role in COVID-19?
« Reply #250 on: May 04, 2020, 04:47:37 pm »
Could Retroviruses Play a Role in COVID-19?   

May 3, 2020

Dr. Joseph Mercola

SNIPPETS:

Judy Mikovits, Ph.D. is a 🔬 cellular and molecular biologist,1 researcher and was the founding research director of the Whittemore Peterson Institute that researches and treats chronic fatigue syndrome (CFS) in Reno, Nevada.

She is likely one of the most qualified scientists in the world to comment on this disease because of her groundbreaking research in molecular biology and virology. Mikovits is absolutely brilliant, but like many gifted researchers, her complex discussions on science quite challenging for the average lay person to follow.

For this reason, I present her interview in a different format, cutting and splicing pieces together to present a more cohesive and coherent presentation of her many important points. I would encourage you to watch the initial, very short, videos first, so you will be well-grounded, and if you are motivated, watch the entire interview at the bottom of this article. ... ...

One of the most shocking revelations Mikovits reveals is that she doesn’t believe SARS-CoV-2 is the cause of COVID-19 but merely serves to activate or wake up a dormant XMRV infection. To support her assertion, she states that COVID-19 patients have the same cytokine signature as the gammaretrovirus XMRV, which she published many years ago.

XMRV stands for “xenotropic murine leukemia virus-related virus.” Xenotrophic refers to viruses that only replicate in cells other than those of the host species. So, XMRVs are viruses that infect human cells yet are not human viruses.2

Full article with videos: 

Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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One Month ago, April 5, 2020, the World Death Count was 4,000 less than US Death Count today. If that continues, we will have over ☠️ 250,000 deaths in the USA by June 5, 2020. 😵


May 5,2020 COVID-19 Deaths per State Now Listed
Click on image below for update:


GATES/CDC “WAR GAMES” PRECEDED PANDEMIC THEIR OWN VIDEO :o

YOU CAN’T MAKE THIS STUFF UP

Gates, CDC, WHO, Pharma and even hotel industry people (!) got together in NYC in November 2019 and “war gamed” the following scenario:

1. Pandemic

2. Kills millions

3. Catastrophic economic shutdown

4. The 😈 need for a global vaccine


You can’t make this up.

It’s their own video.

https://realfoodchannel.com/gates-cdc-war-games-preceded-pandemic/


« Last Edit: May 05, 2020, 02:06:11 pm by AGelbert »
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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Re: COVID-19 🏴☠️ Pandemic
« Reply #252 on: May 06, 2020, 11:42:55 am »
May 6,2020 COVID-19
Click on image below for update:


May 6, 2020
Doctors Speak Out, Ventilators Make Death Rates Soar

A number of published papers have noted ventilators make COVID-19 death risks soar. One report suggests the comparison was 76.4% vs. 19.8% (18-65) and 97.2% vs. 26.6% (65+). Should we be doing high-flow nasal cannulas (HFNC) instead

Read More >>

Quote
Hyperbaric Oxygen Therapy

Sadly missing from the conventional conversation is the use of hyperbaric oxygen therapy (HBOT) which I believe might be an excellent treatment method . As noted by Dr. Andrew Saul, editor-in-chief of the Orthomolecular Medicine News Service, in “A Review of Helpful Antiviral Strategies”:

“Making the oxygen available in a way that's appropriate to the severity of the patient is the answer. We have to remember that our body is singularly good at taking in oxygen or we wouldn't be here. And our lungs have a huge amount of absorptive space. I mean, that's what they do. It's just an extraordinary system that we have.

Oxygen goes in by diffusion. You don't push it in; the body sucks it in because if you have more oxygen outside than you do inside, it just goes through. All you do is give a lot of absorptive surface. And if you flattened out all the little alveoli in the lungs, you'd have an enormous area …

So, by providing the oxygen and then see if the body will take it up, you've made the first step. That can be done preventively by fresh air and exercise and going out and playing …

If somebody needs more oxygen, and you want to give them a little pressure, if that makes the patient better, then you do it. But the idea that you've got to ram this oxygen like a supercharger on a Mustang is, I think, a little bit, shall we say, industry friendly …

[The alveoli] are tiny, tiny little sacks. They have some of the thinnest little membranes you've ever seen. Look at them under a microscope.




They're very delicate. So, the last thing you want to do is add injury to insult.

Agelbert NOTE: For those who haven't been living in a cave without internet for the past three months or so, the fact that COVID-19 causes major damage to the lungs is common knowledge.

However, whether it is from the SARS-CoV-2 virus, and/or some retrovirus latent in us that works with it to cause the lethal cytokine storm (i.e. excessive inflammatory immune response that causes your own immune system to attack healthy cells and kills you if it is not stopped), most people are not aware of an important detail about that lung damaging process that relates to the alveoli.

Yes, the ACE2 receptor on certain lung cells (NOT the alveoli) is attacked to gain entry into said cell and enable the virus to replicate. BUT, something else happens at the same time.

Those ACE2 receptors normally dock with ACE (Angiotensin Converting Enzyme) to lower the blood pressure. With the receptor blocked by the virus, blood pressure does go up, but that ain't all.

When all those ACE proteins routinely dock on the cell ACE2 receptors normally, the lung cell produces surfactant. That is a fancy name for a soaplike substance. NO, it isn't soap. However, the analogy is good because it allows us to think of soap bubbles, which don't burst right away when you blow the bubbles because of surface tension surfactant.
Soap Bubbles

You can blow water with not enough soap all day long through the ring and not get soap bubbles. Any child knows that. Well, when our lung cells are not putting out enough surfactant to adequately coat their alveoli neighbors, the alveoli cannot interchange oxygen well.

WHY?

Because a lot of them collapse like those soap bubbles without enough soap. Then it gets even uglier.

Your body is alive. Your immune system is always checking to see if things are as they should be. Collapsed alveoli release cell chemicals that the immune system detects as a big problem. The immune cell soldiers within the lung (i.e phagocytes) set out to eat them to get them out of the way. So far, so good.

Unfortunately, because the viral infection causes so many alveoli to collapse, the abundance of chemicals from collapsed alveoli floating around confuse the phagocytes into attacking healthy alveoli, that get destroyed along with the collapsed ones. Then it gets even worse!

Lung cell tissue repairs are attempted with a fibrous substance that causes rigidity and even less ability to interchange oxygen. That fibrous substance normally works as a temporary seal which is removed later. Normally, only a small percentage of cells need repairing so their temporary dysfuntion will not threaten the overall lung function. BUT, when so many alveoli cells are being attacked because they are collapsing from not enough surfactant to keep them flexible (flexibility is REQUIRED so they can release CO2 and take up oxygen efficiently 👉 they are constantly either contracting or expanding in size as air pressure increases or decreases from breathing), the immune system, which is now causing all this damage from what is lablelled the cytokine storm, makes things even worse than that!

Large amounts of fluid not normally present in the lungs begins to flood the already partly compromised alveolar sacks. Being effectvely under water, they cannot intake any oxygen. The lungs get waterlogged, requiring MUCH more energy from your diaphragm muscles to expand and contract, which you experience as shortness of breath (dyspnea).

As your diaphragm chest muscles begin to work harder to expand your lungs to get oxygen, your heart beats faster to get any oxygen depleted blood to your lungs and oxygen collected by your lungs to the rest of your body.

To make a virus attack story short, you have got to stop the blocking of the ACE2 receptor, like, yesterday. But, in the meantime, you have got to got to get rid of excess CO2 in all your body tissues AND get sufficient oxygen to them until your lungs are cleared of fluid and your alveoli have sufficient surfactant to oxygenate efficiently without getting hammered by your own immune system soldier lung phagocytes.

Here is where the problem begins in our hospitals in the USA. Doctors have protocols they have developed over the decades that they are required to strictly adhere to or face punishemnt or accusations of malpractice.

The patient that has so much trouble breathing for all the reasons I just went through is experiencing what appears to doctors as ARDS (Acute Respiratory Distress Syndrome). They check your Oxygen Perfusion (i.e. measure the percentage of oxygen in your blood with a clever non-invasive device they put on your finger that measures oxygen level by the color of the blood).

If Oxygen Perfusion is below a certain percentage, they go to their standard ARDS therapy protocol. THAT IS, they put you in ICU on a ventilator. That works well with normal ARDS because, with normal ARDS, a person needs help with their diaphragm musles to breathe. If they don't get that help, they can get heart failure (i.e. the large ventricle in your heart that pumps blood into your body from the lungs gets exhausted, you get a heart attack, and can die).

BUT, putting a person with COVID-19 on a ventilator is a very big mistake because, though COVID-19 patients have ARDS symptoms, they DO NOT actually have ARDS!

WHY? Because there is no ACE2 Blocked Receptor CAUSED REDUCTION IN ALVEOLI SURFACTANT IN NORMAL ARDS! And furthermore, COVID-19 patients DO NOT have "tired" diaphragm muscles or any danger of heart failure (unless they have a pre-existing heart disease co-morbidity, which is not the norm).

That is why doctors, after inadvertently causing the death of tens of thousands of COVID-19 patients, have begun to turn patients face down, so the excess lung fluid does not inhibit oxygenation until the virus can be gotten under control, and, instead of entubing the patient with a ventilator, given them high-flow nasal cannulas (HFNC).

Up until now, when the cytokine storm was destroying lung tissue, the COVID-19 patients were given steroids while on a ventilator. The deal with steroids is that they signal the immune system soldiers that "everything is okay". Thus, the attacks on healthy tissue stop. However, if an effective antiviral like Interferon-alfa-2b is not part of that therapy, the virus will take advantage of the steroidal standing down of the immune system by replicating MORE virus. THAT is most likely the main cause of death of those that that were given steroids in the first week of hospitalization with a serious COVID-19 infection.

I've been reading and listening to lectures on all this. Doctors have figured out how to time the steroids to administer them to patients in the hospital with a serious COVID-19 infection AFTER the first week. If the steroids are given the second week, a greater percentage of patients survive.

They figured all that out before the really smart ones figured out HOW AND WHY a ventilator is a lethally counterproductive COVID-19 therapy. Unfortunately, many hospitals in the USA still haven't figured that out.

As for Interferon-alfa-2b, let us hope that the effectiveness of using this proven antiviral to combat COVID-19 will become the norm. As I posted here recently, there is no question that Interferon-alfa-2b kills the SARS-CoV-2 virus (as well as retroviruses in our system). It has been used for a wide range of indications, including viral infections and cancers.

Quote
So far, two non-peer reviewed research articles have been published. One study at the University of Texas Medical Branch, Galveston, showed evidence of a direct anti-viral effect of Interferon alpha against novel Coronavirus in vitro. The study demonstrated around 10,000 fold reduction in the quantity of virus that was pre-treated with Interferon alpha 48 hours earlier. A second study by universities in China, Australia and Canada analysed 77 moderate COVID-19 subjects in Wuhan and observed that those who received Interferon alpha-2b showed a significant reduction in the duration of virus shedding period and even in levels of the inflammatory cytokine, IL-6. [6] [7]
https://en.wikipedia.org/wiki/Interferon_alfa-2b
« Last Edit: May 06, 2020, 10:39:23 pm by AGelbert »
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

AGelbert

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May 6, 2020

Doctors Speak Out, Ventilators Make Death Rates Soar

A number of published papers have noted ventilators make COVID-19 death risks soar. One report suggests the comparison was 76.4% vs. 19.8% (18-65) and 97.2% vs. 26.6% (65+). Should we be doing high-flow nasal cannulas (HFNC) instead


Read More >>

Quote
Hyperbaric Oxygen Therapy

Sadly missing from the conventional conversation is the use of hyperbaric oxygen therapy (HBOT) which I believe might be an excellent treatment method . As noted by Dr. Andrew Saul, editor-in-chief of the Orthomolecular Medicine News Service, in “A Review of Helpful Antiviral Strategies”:

“Making the oxygen available in a way that's appropriate to the severity of the patient is the answer. We have to remember that our body is singularly good at taking in oxygen or we wouldn't be here. And our lungs have a huge amount of absorptive space. I mean, that's what they do. It's just an extraordinary system that we have.

Oxygen goes in by diffusion. You don't push it in; the body sucks it in because if you have more oxygen outside than you do inside, it just goes through. All you do is give a lot of absorptive surface. And if you flattened out all the little alveoli in the lungs, you'd have an enormous area …

So, by providing the oxygen and then see if the body will take it up, you've made the first step. That can be done preventively by fresh air and exercise and going out and playing …

If somebody needs more oxygen, and you want to give them a little pressure, if that makes the patient better, then you do it. But the idea that you've got to ram this oxygen like a supercharger on a Mustang is, I think, a little bit, shall we say, industry friendly …

[The alveoli] are tiny, tiny little sacks. They have some of the thinnest little membranes you've ever seen. Look at them under a microscope.




They're very delicate. So, the last thing you want to do is add injury to insult.

Agelbert NOTE: For those who haven't been living in a cave without internet for the past three months or so, the fact that COVID-19 causes major damage to the lungs is common knowledge.

However, whether it is from the SARS-CoV-2 virus, and/or some retrovirus latent in us that works with it to cause the lethal cytokine storm (i.e. excessive inflammatory immune response that causes your own immune system to attack healthy cells and kills you if it is not stopped), most people are not aware of an important detail about that lung damaging process that relates to the alveoli.

Yes, the ACE2 receptor on certain lung cells (NOT the alveoli) is attacked to gain entry into said cell and enable the virus to replicate. BUT, something else happens at the same time.

Those ACE2 receptors normally dock with ACE (Angiotensin Converting Enzyme) to lower the blood pressure. With the receptor blocked by the virus, blood pressure does go up, but that ain't all.

When all those ACE proteins routinely dock on the cell ACE2 receptors normally, the lung cell produces surfactant. That is a fancy name for a soaplike substance. NO, it isn't soap. However, the analogy is good because it allows us to think of soap bubbles, which don't burst right away when you blow the bubbles because of surface tension surfactant.
Soap Bubbles

You can blow water with not enough soap all day long through the ring and not get soap bubbles. Any child knows that. Well, when our lung cells are not putting out enough surfactant to adequately coat their alveoli neighbors, the alveoli cannot interchange oxygen well.

WHY?

Because a lot of them collapse like those soap bubbles without enough soap. Then it gets even uglier.

Your body is alive. Your immune system is always checking to see if things are as they should be. Collapsed alveoli release cell chemicals that the immune system detects as a big problem. The immune cell soldiers within the lung (i.e phagocytes) set out to eat them to get them out of the way. So far, so good.

Unfortunately, because the viral infection causes so many alveoli to collapse, the abundance of chemicals from collapsed alveoli floating around confuse the phagocytes into attacking healthy alveoli, that get destroyed along with the collapsed ones. Then it gets even worse!

Lung cell tissue repairs are attempted with a fibrous substance that causes rigidity and even less ability to interchange oxygen. That fibrous substance normally works as a temporary seal which is removed later. Normally, only a small percentage of cells need repairing so their temporary dysfuntion will not threaten the overall lung function. BUT, when so many alveoli cells are being attacked because they are collapsing from not enough surfactant to keep them flexible (flexibility is REQUIRED so they can release CO2 and take up oxygen efficiently 👉 they are constantly either contracting or expanding in size as air pressure increases or decreases from breathing), the immune system, which is now causing all this damage from what is lablelled the cytokine storm, makes things even worse than that!

Large amounts of fluid not normally present in the lungs begins to flood the already partly compromised alveolar sacks. Being effectvely under water, they cannot intake any oxygen. The lungs get waterlogged, requiring MUCH more energy from your diaphragm muscles to expand and contract, which you experience as shortness of breath (dyspnea).

As your diaphragm chest muscles begin to work harder to expand your lungs to get oxygen, your heart beats faster to get any oxygen depleted blood to your lungs and oxygen collected by your lungs to the rest of your body.

To make a virus attack story short, you have got to stop the blocking of the ACE2 receptor, like, yesterday. But, in the meantime, you have got to got to get rid of excess CO2 in all your body tissues AND get sufficient oxygen to them until your lungs are cleared of fluid and your alveoli have sufficient surfactant to oxygenate efficiently without getting hammered by your own immune system soldier lung phagocytes.

Here is where the problem begins in our hospitals in the USA. Doctors have protocols they have developed over the decades that they are required to strictly adhere to or face punishemnt or accusations of malpractice.

The patient that has so much trouble breathing for all the reasons I just went through is experiencing what appears to doctors as ARDS (Acute Respiratory Distress Syndrome). They check your Oxygen Perfusion (i.e. measure the percentage of oxygen in your blood with a clever non-invasive device they put on your finger that measures oxygen level by the color of the blood).

If Oxygen Perfusion is below a certain percentage, they go to their standard ARDS therapy protocol. THAT IS, they put you in ICU on a ventilator. That works well with normal ARDS because, with normal ARDS, a person needs help with their diaphragm musles to breathe. If they don't get that help, they can get heart failure (i.e. the large ventricle in your heart that pumps blood into your body from the lungs gets exhausted, you get a heart attack, and can die).

BUT, putting a person with COVID-19 on a ventilator is a very big mistake because, though COVID-19 patients have ARDS symptoms, they DO NOT actually have ARDS!

WHY? Because there is no ACE2 Blocked Receptor CAUSED REDUCTION IN ALVEOLI SURFACTANT IN NORMAL ARDS!  And furthermore, COVID-19 patients DO NOT have "tired" diaphragm muscles or any danger of heart failure (unless they have a pre-existing heart disease co-morbidity, which is not the norm).

That is why doctors, after inadvertently causing the death of tens of thousands of COVID-19 patients, have begun to turn patients face down, so the excess lung fluid does not inhibit oxygenation until the virus can be gotten under control, and, instead of entubing the patient with a ventilator, given them high-flow nasal cannulas (HFNC).

Up until now, when the cytokine storm was destroying lung tissue, the COVID-19 patients were given steroids while on a ventilator. The deal with steroids is that they signal the immune system soldiers that "everything is okay". Thus, the attacks on healthy tissue stop. However, if an effective antiviral like Interferon-alfa-2b is not part of that therapy, the virus will take advantage of the steroidal standing down of the immune system by replicating MORE virus. THAT is most likely the main cause of death of those that that were given steroids in the first week of hospitalization with a serious COVID-19 infection.

I've been reading and listening to lectures on all this. Doctors have figured out how to time the steroids to administer them to patients in the hospital with a serious COVID-19 infection AFTER the first week. If the steroids are given the second week, a greater percentage of patients survive.

They figured all that out before the really smart ones figured out HOW AND WHY a ventilator is a lethally counterproductive COVID-19 therapy. Unfortunately, many hospitals in the USA still haven't figured that out.

As for Interferon-alfa-2b, let us hope that the effectiveness of using this proven antiviral to combat COVID-19 will become the norm. As I posted here recently, there is no question that Interferon-alfa-2b kills the SARS-CoV-2 virus (as well as retroviruses in our system). It has been used for a wide range of indications, including viral infections and cancers.

Quote
So far, two non-peer reviewed research articles have been published. One study at the University of Texas Medical Branch, Galveston, showed evidence of a direct anti-viral effect of Interferon alpha against novel Coronavirus in vitro. The study demonstrated around 10,000 fold reduction in the quantity of virus that was pre-treated with Interferon alpha 48 hours earlier. A second study by universities in China, Australia and Canada analysed 77 moderate COVID-19 subjects in Wuhan and observed that those who received Interferon alpha-2b showed a significant reduction in the duration of virus shedding period and even in levels of the inflammatory cytokine, IL-6. [6] [7]
https://en.wikipedia.org/wiki/Interferon_alfa-2b
« Last Edit: May 06, 2020, 10:38:46 pm by AGelbert »
Rob not the poor, because he is poor: neither oppress the afflicted in the gate:
For the Lord will plead their cause, and spoil the soul of those that spoiled them. Pr. 22:22-23

Surly1

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It's a shame it has come to this, but it has. The aggressive virus slurpers are on the march. Some call Covid-19 the "boomer remover."

Face masks make a political statement in era of coronavirus




WASHINGTON (AP) — The decision to wear a mask in public is becoming a political statement — a moment to pick sides in a brewing culture war over containing the coronavirus.

While not yet as loaded as a “Make America Great Again” hat, the mask is increasingly a visual shorthand for a debate pitting those willing to follow health officials’ guidance and cover their faces against those who feel it violates their freedom or buys into a threat they think is overblown.

That resistance is fueled by some of the same people who object to other virus restrictions. The push back has been stoked by President Donald Trump — he didn’t wear a mask during a Tuesday appearance at a facility making them — and some other Republicans, who have flouted rules and questioned the value of masks. It’s a development that has worried experts as Americans are increasingly returning to public spaces.

“There’s such a strong culture of individualism that, even if it’s going to help protect them, people don’t want the government telling them what to do,” said Linsey Marr, a Virginia Tech engineering professor with experience in airborne transmission of viruses.

Inconclusive science and shifting federal guidance have no doubt muddied the political debate. Health officials initially said wearing masks was unnecessary, especially amid a shortage of protective materials. But last month, the Centers for Disease Control and Prevention began recommending wearing cloth masks in public to prevent transmitting the virus to others.

Whether Americans are embracing the change may depend on their political party. While most other protective measures like social distancing get broad bipartisan support, Democrats are more likely than Republicans to say they’re wearing a mask when leaving home, 76% to 59%, according to a recent poll by The Associated Press-NORC Center for Public Affairs Research.

The split is clear across several demographics that lean Democratic. People with college degrees are more likely than those without to wear masks when leaving home, 78% to 63%. African Americans are more likely than either white people or Hispanic Americans to say they’re wearing masks outside the home, 83% to 64% and 67%, respectively.

The notable exception is among older people, a group particularly vulnerable to serious illness from the virus. Some 79% of those age 60 and over were doing so compared with 63% of those younger.

“Who knows what the truth is on masks?” asked Republican Kentucky Sen. Rand Paul, who, unlike some of his colleagues, went without a mask Tuesday in the Senate. Paul already contracted the virus and believes he is no longer contagious.

His comments were a long way from New York Gov. Andrew Cuomo’s moral argument for the mask a few days earlier.

“How people cannot wear masks — that to me is even disrespectful,” Cuomo said. “You put so many people at risk because you did not want to wear a mask?”

Effectiveness aside, politicians of both parties are clued into the powerful symbolism of the mask, and many Americans take their cues from the president.

Trump was barefaced when he spoke to masked journalists, workers and Secret Service agents at the Arizona factory Tuesday. He later said he briefly wore a mask backstage but took it off because facility personnel told him he didn’t need it.

But Trump has been mask averse for weeks. Within minutes of the CDC announcing its updated mask recommendations, he said, “I don’t think that I’m going to be doing it.”

Trump has told advisers that he believes wearing one would “send the wrong message,” according to one administration and two campaign officials not authorized to publicly discuss private conversations. The president said doing so would make it seem like he is preoccupied with health instead of focused on reopening the nation’s economy — which his aides believe is the key to his reelection chances in November.

Moreover, Trump, who is known to be especially cognizant of his appearance on television, has also told confidants that he fears he would look ridiculous in a mask and the image would appear in negative ads, according to one of the officials.

“It’s a vanity thing, I guess, with him,” House Speaker Nancy Pelosi said of Trump on MSNBC. “You’d think, as the president of the United States, you would have the confidence to honor the guidance he’s giving the country.”

That’s left those around him unsure of how to proceed. White House aides say the president hasn’t told them not to wear them, but few do. Some Republican allies have asked Trump’s campaign how it would be viewed by the White House if they were spotted wearing a mask, according to two campaign officials who spoke on condition of anonymity because they weren’t authorized to discuss private conversations.

Meanwhile, Trump’s reelection campaign has ordered red Trump-branded masks for supporters and is considering giving them away at events or in return for donations. But some advisers are concerned the president will later sour on the idea, according to one campaign official.

That uncertainty was on display last week, when Vice President Mike Pence went maskless at the Mayo Clinic in Minnesota. He later acknowledged he should have worn one and did use a mask during a subsequent trip to a ventilator plant.

The issue has been far less fraught for Democrats, whose presumptive presidential nominee, Joe Biden, has said he wears a mask when interacting with the Secret Service.

Dilemmas for politicians and other Americans are only going to increase as parts of the country begin easing stay-at-home orders and businesses reopen with new rules. The tensions have already flared in Michigan, where a man was shot and killed over a mask dispute at a store.

One of the earliest communities to require masks in public was Laredo, Texas. A $1,000 noncompliance fine was negated by an order from the governor, but Mayor Pete Saenz said his community is still asking citizens to comply so hospitals aren’t overtaxed with new cases.

“We don’t want to violate anyone’s civil liberties,” Saenz said. But “we can’t help you, if it’s beyond our medical capacity, whether you exercise your civil liberties or not.”
« Last Edit: May 07, 2020, 11:40:56 am by AGelbert »

 

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