new deadly human-to-human-transmissible coronavirus emerges out of China
POSTED BY: 1KIKI
UPDATED: Tuesday, May 5, 2026 22:21
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097694#1097694 and includes 4 posts that are:
world - countries with greater than 5,000 total cases
US
&
states with greater than 3,000 total cases
California
Los Angeles County
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They've done testing on ferrets and ... something else, I forget which. Safety testing in people is the next step.
But how do you test for effectiveness, short of exposing people to the virus? There's no guarantee that another animal's immune response is a good model for ours.
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Oh, dear. I heard about this on Chris Martensen's "Peak Prosperity" and looked it up to make sure
Quote:
Novel coronavirus attacks and destroys T cells, just like HIV
Angela Betsaida B. Laguipo, BSNBy Angela Betsaida B. Laguipo, BSNApr 13 2020
The immune system has many components that work together in protecting the body from foreign invaders. One of the most important types of immune cells is T lymphocytes or T cells, a type of white blood cell that acts as the core of adaptive immunity, the system that modifies the immune response to specific pathogens.
Now, a team from the United States and China revealed evidence that the coronavirus disease, caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), attacks the immune system’s T lymphocytes. The worrying findings highlight the destructive power of the novel coronavirus, which can destroy the immune system, leaving the patient unable to fight off the infection.
Coronaviruses have been causing problems in humans for a long time. Though many versions of the virus are known to trigger only mild symptoms such as common colds. However, three recent types of coronavirus have caused deadly diseases – the severe acute respiratory syndrome (SARS) in China in 2002, the Middle East respiratory syndrome (MERS) in Saudi Arabia in 2012, and the current global pandemic, the coronavirus disease (COVID-19), which first emerged in Wuhan City, Hubei Province, in China December 2019.
The impact of the previous coronavirus outbreaks in 2002 and 2012 has been mild compared with the mayhem unleashed by the SARS-CoV-2. Within only a few months, the novel coronavirus has prompted most countries to go into lockdown, dwindling economies, and overwhelming health care systems with the more than 2 million people infected.
Meanwhile, scientists across the globe are racing to understand the SARS-CoV-2-in the hope of finding a treatment or cure. Now, the researchers’ surprise discovery has shed light on the potency of the novel coronavirus is killing powerful immune cells, which are supposed to kill the virus instead.
The researchers from the Fudan University in Shanghai, China, and the New York Blood Centre, has studied the virus’s action on T-lymphocyte cell lines. T lymphocytes or T cells work by identifying and eliminating foreign invaders in the body.
To arrive at their findings, published in the journal of Cellular & Molecular Immunology, the team captured a cell infected by the virus, penetrated the membrane, and injected toxic chemicals into the cell. After this, the chemicals killed both the virus and infected cells by tearing them into pieces.
Surprisingly, the team has found that when the coronavirus and the T cell came into contact with each other, the T cell became prey to the coronavirus, wherein a structure in the spike of the coronavirus triggered the attachment of a viral envelope and the cell membrane. After, the genes of the virus entered the T cell and overwhelmed it, took it hostage, and deactivated its ability to protect the body.
The team then tried to do the same with the SARS virus, and another coronavirus, but these pathogens were not able to infect T cells. The researchers suspect that the SARS virus, which caused an outbreak in 2002 to 2003, has a lack of a membrane fusion function. The virus can only infect cells that have a particular receptor protein called the angiotensin-converting enzyme 2 (ACE2). T cells contain only a few ACE2 receptor proteins.
It is an important discovery, knowing the effect of the SARS-CoV-2 on T cells, since this may show why the disease is spreading so quickly, and infecting so many across the globe. It also explains why certain vulnerable populations are at a high risk of dying from the infection, including those who are more than 65, those who are immunocompromised, and those with underlying medical conditions like lung disease, heart disease, diabetes, and hypertension.
Further investigation shows that patients who died from COVID-19 had damage to theirNOTIFY: Y | REPLY | REPLY WITH QUOTE | PERMALINK | TOP | HOME
HOLY CRAP.
This should be headline news everywhere.
"Also, the team found that unlike HIV that replicates faulty T cells, the coronavirus does not replicate, showing that the T cells and the virus may end up dying together."
Well, HIV is a retrovirus, which means it creates DNA from its RNA code, and then inserts its DNA into the human DNA at random points. So when HIV-infected T-cells replicate, they replicate the HIV genes along with their own T-cell DNA. Since SARS-COV-2 ISN'T a retrovirus it shouldn't be able to do that.
Still, HOLY CRAP.
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But there was an link of good news buried in the bad ...
Quote:MORE AT https://www.news-medical.net/news/20200406/Experimental-drug-APN0
Experimental drug APN01 prevents COVID-19 infection in the lab
Dr. Ananya Mandal, MDBy Dr. Ananya Mandal, MDApr 6 2020
With the world gripped with the COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there is a frantic rush to find an effective drug that can be used to treat the disease.
Researchers from the University of British Columbia, in collaboration with others, have found an experimental drug that can inhibit the SARS-CoV-2 virus from infecting host cells. Their study titled, "Inhibition of SARS-CoV-2 infections in engineered human tissues using clinical-grade soluble human ACE2," was published in the latest issue of the journal Cell.
... Dr. Josef Penninger, study leader, and his team are working on ways to inhibit SARS-CoV-2's capacity to infect human host cells. They write that in their previous study, they had explained the mechanism of infection caused by this virus and how angiotensin-converting enzyme 2 (ACE2) receptor plays a vital role in the infection. The enzyme ACE2 has the capacity to protect the lungs from injury caused by the virus. This also provided an explanation regarding the severe lung damage, respiratory failure, kidney and blood vessels, and eventual death seen in some of the individuals.
... Dr. Art Slutsky, a scientist at the Keenan Research Centre for Biomedical Science of St. Michael's Hospital and professor at the University of Toronto, who was part of this study explained, "Our new study provides very much needed direct evidence that a drug -- called APN01 (human recombinant soluble angiotensin-converting enzyme 2 - hrsACE2) -- soon to be tested in clinical trials by the European biotech company Apeiron Biologics, is useful as an antiviral therapy for COVID-19."
APN01 is a recombinant human Angiotensin Converting Enzyme 2 (rhACE2) under Phase-2 clinical development in ALI (Acute Lung Injury) and PAH (Pulmonal arterial hypertension). Recently, ACE2 has been shown to be the cellular entry receptor for the novel coronavirus SARS-CoV-2. Therefore APEIRON initiated now a clinical Phase II study in Austria, Germany, and Denmark for treatment of COVID-19 and is planning a clinical study in China in patients infected with SARS-CoV-2. APEIRON Biologics AG.
For this study, the team used biomedically engineered organoids in the lab that mimicked human blood vessels and kidneys. These are essentially clumps of cells that act as the whole organ within the human body and are grown from human stem cells. On these organoids, the team then used hrsACE2 and found that it could prevent the entry of the coronavirus into the host cells. The decrease in the viral load affecting the host cells was by a factor of 1,000-5,000, they wrote.
... For this study, they used a Swedish patient who tested positive for COVID-19 in early February 2020. The SARS-CoV-2 virus was isolated from the nasopharyngeal samples of the patient. They grew the virus in the Vero E6 cells and looked at its genetic sequence using Next-Generation Sequencing (Genbank accession number MT093571).
... They wrote, "hrsACE-2 can inhibit SARS-CoV-2 infection in a dose-dependent manner hrsACE2 has already undergone clinical phase 1 and phase 2 testing and is being considered for the treatment of COVID-19."
The study was funded by the Canadian federal government.
Sources:
Zhang, H., Penninger, J.M., Li, Y., Zhong, N., and Slutsky, A.S. (2020). Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med.
APEIRON’s product pipeline - https://www.apeiron-biologics.com/project-overview/#APN01
APEIRON Biologics Initiates Phase II Clinical Trial of APN01 for Treatment of COVID-19 - https://www.apeiron-biologics.com/wp-content/uploads/2020/04/20200402_
APEIRON_Phase-2-EU-trial_APN01_ENG.pdf
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FANTASTIC!
BUT ... your original link has seriously bad implications for anyone already infected. If you can't ramp up T-cell production AND educate them fast enough to get ahead of the virus, it's like your immune system has Alzheimer's and is being mowed down by machine guns at the same time.
AND ... your original link indicates T-cells have few ACE-2 receptors. So this potential treatment, while it may be able to reduce the overall viral load, doesn't seem protective of T-cells. It would be a race in terms of which happens fastest - viral load reduction or T-cell infection.
BTW - perhaps the T-cell infection happens because of those non-existent HIV-like spike protein inserts. In which case, one would also need to block attachment at the spike proteins for good results across a population.
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Quote:HAHAHAHA!
non-existent HIV-like spike protein inserts.
I've been thinking about that paper ever since it came out.
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If we did not MAKE men poor - William Blake
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Newsom's conditions for reopening CA:
Quote:
No. 1. Public health authorities [must] posses the ability to test people and track contacts of new cases is condition
2 ... taking more steps to protect the vulnerable and the elderly.[SUCH AS?]
3 ... bolster state hospital systems and build up supplies of PPE.
4 ... "engage researchers and universities" to work toward treatments.
5 ... is re-drawing floor plans in businesses, parks etc. to accommodate distancing. And finally, the ability to switch the 'stay at home' order back on if the second wave begins to overwhelm.
What about WEARING MASKS???
You can't get to condition #1 until you have (a) enough test kits to test a lot of people AND (b) the number of cases has fallen low enough that tracing contacts is even possible. And you have to find some way to track the homeless and illegals. Condition #1 seems unachievable except in the long term, maybe.
Taking more steps to protect the vulnerable and elderly? Like ... how?
The rest is just blue-sky thinking in an ideal world. If Newsom follows his own plan, CA will NEVER re-open. In the meantime, will the Federal government continue to back an open-ended loan program?
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Pity would be no more,
If we did not MAKE men poor - William Blake
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Quote:
Originally posted by SIGNYM:
They've done testing on ferrets and ... something else, I forget which. Safety testing in people is the next step.
But how do you test for effectiveness, short of exposing people to the virus? There's no guarantee that another animal's immune response is a good model for ours.
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Pity would be no more,
If we did not MAKE men poor - William Blake
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I volunteer. Give it to me.
Unfortunately, I'm about 99% sure I've already had it.
Do Right, Be Right. :)
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Quote:I can imagine a quick initial test -
Originally posted by SIGNYM:
They've done testing on ferrets and ... something else, I forget which. Safety testing in people is the next step.
But how do you test for effectiveness, short of exposing people to the virus? There's no guarantee that another animal's immune response is a good model for ours.
-----------
Pity would be no more,
If we did not MAKE men poor - William Blake
#STAYTHEFUCKHOME
#WEARAMASK
vaccinate people
look for antibodies and levels of antibodies, since some people seem to make more than others
isolate those antibodies and mix them with a dose of virus, with the virus '#virus particles dose' calculated to be less than the '#antibodies dose' by a safe amount
all of the virus particles in the mix should then be coated with antibodies
dose uninfected ferrets with the mix
if the antibodies are neutralizing, the ferrets should stay healthy
ETA: It's simple in concept, but extremely technical and demanding in execution. Still, it could be a reasonable intermediate step.
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