Monday, 3 May 2021

Malevolent Designer News - Why SARS-CoV-2 is Deadly and Different

New Cell Atlas of COVID Lungs Reveals Why SARS-CoV-2 is Deadly and Different | Columbia University Irving Medical Center

Creationist mode:


News today shows just how amazingly brilliant the Intelligent [sic] Designer who designed the SARS-C0V-2 virus to kill as many people as possible was. Scientists at Columbia University's Irving Medical Center have shown how it is far more deadly and has a longer-lasting effect on survivors than other similar viruses.

According to the Columbia University news release:
Led by researchers at Columbia University Vagelos College of Physicians and Surgeons and Herbert Irving Comprehensive Cancer Center, the study found that in patients who died of the infection, COVID-19 unleashed a detrimental trifecta of runaway inflammation, direct destruction and impaired regeneration of lung cells involved in gas exchange, and accelerated lung scarring.

Though the study looked at lungs from patients who had died of the disease, it provides solid leads as to why survivors of severe COVID may experience long-term respiratory complications due to lung scarring.
Such is the importance of this work to efforts to fight the current pandemic, that an unedited copy of the paper, which has been accepted for publication, but before formal editing, proof-reading and final corrections, has been made available in Nature, sadly, behind a paywall.

It’s a devastating disease, but the picture we’re getting of the COVID-19 lung is the first step towards identifying potential targets and therapies that disrupt some of the disease’s vicious circuits. In particular, targeting cells responsible for pulmonary fibrosis early on could possibly prevent or ameliorate long-term complications in survivors of severe COVID-19

A normal lung will have many of the same cells we find in COVID, but in different proportions and different activation states. In order to understand how COVID-19 is different compared to both control lungs and other forms of infectious pneumonias, we needed to look at thousands of cells, one by one.

In COVID-19, we see expansion and uncontrolled activation of macrophages, including alveolar macrophages and monocyte-derived macrophages. They are completely out of balance and allow inflammation to ramp up unchecked. This results in a vicious cycle where more immune cells come in causing even more inflammation, which ultimately damages the lung tissue.

Unlike other cytokines such as IL-6, which appears to be universally prevalent in various pneumonias, IL-1ß production in macrophages is more pronounced in COVID-19 compared to other viral or bacterial lung infections. That’s important because drugs exist that tamp down the effects of IL-1ß.

Among others, IL-1ß appears to be a culprit in inducing and maintaining this intermediate cell state, thereby linking inflammation and impaired lung regeneration in COVID-19. This suggests that in addition to reducing inflammation, targeting IL-1ß may help take the brakes off cells required for lung repair.

This analysis predicted that inhibition of STAT signaling could alleviate some of the deleterious effects caused by pathological fibroblasts. Our hope is that by sharing this analysis and massive data resource, other researchers and drug companies can begin to test and expand on these ideas and find treatments to not only treat critically ill patients, but also reduce complications in people who survive severe COVID-19.

Dr. Benjamin Izar, MD
Assistant professor
Columbia University Irving Cancer Center,
New York, NY, USA
In their abstract, the authors say their 'integrated analysis' revealed:
...significant alterations in cellular composition, transcriptional cell states, and cell-to-cell interactions, providing insights into the biology of lethal COVID-19. COVID-19 lungs were highly inflamed with dense infiltration of aberrantly activated monocyte-derived macrophages and alveolar macrophages, but demonstrated impaired T cell responses. Monocyte/macrophage-derived IL-1β and epithelial cell-derived IL-6 were unique features of SARS-CoV-2 infection compared to other viral and bacterial causes of pneumonia. Alveolar type 2 cells adopted an inflammation-associated transient progenitor cell state and failed to undergo full transition into alveolar type 1 cells resulting in impaired lung regeneration.
The Columbia University press release continues:
“It’s a devastating disease, but the picture we’re getting of the COVID-19 lung is the first step towards identifying potential targets and therapies that disrupt some of the disease’s vicious circuits. In particular, targeting cells responsible for pulmonary fibrosis early on could possibly prevent or ameliorate long-term complications in survivors of severe COVID-19,” says Benjamin Izar, MD, PhD, assistant professor of medicine, who led a group of more than 40 investigators to complete in several months a series of analyses that usually takes years.

This study and a companion paper led by researchers at Harvard/MIT, to which the Columbia investigators also contributed, were published in the journal Nature on April 29.

Study creates atlas of cells in COVID lung


The new study is unique from other investigations in that it directly examines lung tissue (rather than sputum or bronchial washes) using single-cell molecular profiling that can identify each cell in a tissue sample and record each cell’s activity, resulting in an atlas of cells in COVID lung.

“A normal lung will have many of the same cells we find in COVID, but in different proportions and different activation states,” Izar says. “In order to understand how COVID-19 is different compared to both control lungs and other forms of infectious pneumonias, we needed to look at thousands of cells, one by one.”

Izar’s team examined the lungs of 19 individuals who died of COVID-19 and underwent rapid autopsy (within hours of death)—during which lung and other tissues were collected and immediately frozen—and the lungs of non-COVID-19 patients. In collaboration with investigators at Cornell University, the researchers also compared their findings to lungs of patients with other respiratory illnesses.

Drugs targeting IL-1ß may reduce inflammation


Compared to normal lungs, lungs from the COVID patients were filled with immune cells called macrophages, the study found.

Typically during an infection, these cells chew up pathogens but also regulate the intensity of inflammation, which also helps in the fight.

The lungs of patients with COVID-19 have more monocytes expressing IL-1beta than lungs from patients with other respiratory conditions.
Image: Benjamin Izar.
“In COVID-19, we see expansion and uncontrolled activation of macrophages, including alveolar macrophages and monocyte-derived macrophages,” Izar says. “They are completely out of balance and allow inflammation to ramp up unchecked. This results in a vicious cycle where more immune cells come in causing even more inflammation, which ultimately damages the lung tissue.”

One inflammatory cytokine in particular, IL-1ß, is produced at a high rate by these macrophages.

“Unlike other cytokines such as IL-6, which appears to be universally prevalent in various pneumonias, IL-1ß production in macrophages is more pronounced in COVID-19 compared to other viral or bacterial lung infections,” Izar says. “That’s important because drugs exist that tamp down the effects of IL-1ß.”

Some of these drugs are already being tested in clinical trials of COVID patients.

Severe COVID also prevents lung repair


In a typical infection, a virus damages lung cells, the immune system clears the pathogen and the debris, and the lung regenerates.

But in COVID, the new study found that not only does SARS-CoV-2 virus destroy alveolar epithelial cells important for gas exchange, the ensuing inflammation also impairs the ability of the remaining cells to regenerate the damaged lung.
Lung cells in patients with severe COVID become trapped in a state (indicated by the green color) that prevents the cells from repairing damage caused by the infection. The left image shows cells from a healthy lung; the right image shows lung cells from a patient who died from COVID-19.

Images: Benjamin Izar / Columbia University Vagelos College of Physicians and Surgeons.
Though the lung still contains cells that can do the repairs, inflammation permanently traps these cells in an intermediate cell state and leaves them unable to complete the last steps of differentiation needed for replacement of mature lung epithelium.

“Among others, IL-1ß appears to be a culprit in inducing and maintaining this intermediate cell state,” says Izar, “thereby linking inflammation and impaired lung regeneration in COVID-19. This suggests that in addition to reducing inflammation, targeting IL-1ß may help take the brakes off cells required for lung repair.”

Preventing accelerated fibrosis


The researchers also found a large number of specific fibroblast cells, called pathological fibroblasts, that create rapid scarring in COVID-19 lungs. When the fibroblast cells fill the lung with scar tissue, a process called fibrosis, the lung has less space for cells involved in gas exchange and is permanently damaged.

Given the importance of pathological fibroblasts in the disease, Izar’s team closely analyzed the cells to uncover potential drug targets. An algorithm called VIPER, developed previously by Andrea Califano, Dr, chair of systems biology at Columbia University Vagelos College of Physicians and Surgeons, identified several molecules in the cells that play an important role and could be targeted by existing drugs.

“This analysis predicted that inhibition of STAT signaling could alleviate some of the deleterious effects caused by pathological fibroblasts,” Izar says.

“Our hope is that by sharing this analysis and massive data resource, other researchers and drug companies can begin to test and expand on these ideas and find treatments to not only treat critically ill patients, but also reduce complications in people who survive severe COVID-19.”
Very clearly then, the Creationism's brilliant Intelligent [sic] Designer, of whom they should be very proud, if not more than a little embarrassed by its sheer hateful malevolence, has excelled itself and created a nasty little virus with capabilities that tax even the finest scientific brains to understand and bring under some sort of control.

In the SARS-CoV-2 virus and the devastating disease, Covid-19, that it causes, Creationism's pet god has created something only surpassed by Yersinia pestis - the bacterium that killed about 25% of the world's population in the early Medieval Black Death and bubonic plagues that used to sweep the world in successive waves. To date, SARS-CoV-2 has infected just under 153,000,000 people and killed 3,200,000 of them, according to Johns Hopkins Coronavirus Resource Center. 32.4 million of these and 550,000 deaths have been in the USA. India is currently recording in excess of 400,000 new cases daily and can't supply the overwhelmed hospitals with enough oxygen for them.

Of those who survived it, very many have been left with long-term and potentially life-limiting disabilities.

And allegedly all due to the brilliance of Creationism's Intelligent [sic] Designer whom Creationists believe is the supposed God of love and compassion they read about in their Bibles - the god who once drowned everyone and who ordered frequent genocides, according to its Early Iron Age biographers.

Creationist mode:


The abiding mystery, which we are no closer to solving in all this, is why Creationists prefer we all think of their creator god as this malevolent, pestilential, hateful, sadist who evidently hates its creation and enjoys seeing it suffer, rather than accept that a far more sensible, scientific explanation - evolution - is the only explanation that doesn't leave their favourite god looking so awful.


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