2019-nCoV Coronovirus (COVID-19]

COVID has not even a quarter of the US Civil War death count. here in the States that is.

this is so amusing. shenanigans have doubled in my book.

 

Does this mean businesses also have a right to not bake a gay wedding cake too?

 

Yeah, it was about 2% of the population at the time

Which is crazy

https://www.google.com/amp/s/www.history.com/.amp/news/civil-war-deadlier-than-previously-thought

 

I lol'd at the meme telling the B in GLBT that you can't have it both ways

 

7th July. The virus itself isn't killing people


Effects of Viral Infections
Viral infections cause inflammation and injury to various tissues and organs, mostly due to cell death. The mechanisms behind this damage include direct toxicity caused by the presence and replication of the virus, the side-effects of the immune response to the virus, and the consequence of abnormal immune responses to the virus. In most cases, the patient builds resilience by resistance to the infection. This is defined as the ability to limit the viral load so as to protect the body against injury.

On the other hand, the researchers say, tolerance to the pathogen is another mechanism that prevents organ damage and hyperinflammatory responses to the virus. This is described as the physiological pathway by which the body limits the generation of harmful inflammatory chemicals as well as of chemokines produced as a result of the detection of the virus by the body’s immune cells.




Faulty immune response to SARS-CoV-2 one of the main causes of death


Inflammation of the Lung and Fatality in COVID-19
It is established that severe or fatal cases of COVID-19 are linked with the occurrence of hyper-inflammation, which is a cause of organ damage and death. In most cases, fatal COVID-19 is the result of reduced oxygenation of blood below the critical threshold at which it no longer supports function and life. Recent studies have demonstrated the positive role of dexamethasone, a commonly available corticosteroid, in blunting the edge of this inflammatory response and preventing many deaths.

The inference is that lung inflammation is a fundamental cause of death. This, in turn, suggests that tolerance is probably crucial in promoting recovery from COVID-19. It does not, however, show the cause of such inflammation – is it direct injury or the result of an independent and abnormal immune process?

While COVID-19 is an illness of the respiratory tract, recent studies show that the virus infects many tissues outside the lung. The unsolved issue is whether these organs are also injured or inflamed, as shown by histological evidence and clinical features.


Organ Infection Not Linked to Direct Injury
The researchers describe most organs as uninflamed or little inflamed, while evidence of earlier illness was often present. The higher the systemic illness, the worse was the injury to the organ. Thus, patients on the ventilator often had acute tubular necrosis of the kidney.

The presence of the virus in tissues other than the lung was not a measure of the intensity of inflammation or of acute damage to these organs, such as the heart, liver, intestine, or kidney.

Virus Does Not Directly Cause Lung Injury
Even in the lung, the presence of the virus did not relate to pulmonary inflammation in the same areas. Both infected and uninfected areas showed diffuse alveolar damage and bronchopneumonia or appeared utterly normal in some cases.

Other findings included lung clots, mostly mixed, occurring in both small and big vessels. Patches of vasculitis featuring the infiltration of mononuclear cells were found, mostly in the intima (the innermost coat of an organ). Inflamed vessels in these patients did not show the presence of the S protein.

Bronchoalveolar lavage fluid (BALF) has been used for transcription studies on T cells and resident lung macrophages. These show higher numbers of CD8 T cells with fewer resident lung macrophages but may reflect only luminal pathology. The current study, therefore, looked at the phenotypes of the immune cells within whole lung tissue, finding the most striking increase in immune cells to be within the lung parenchyma and not within or around the blood vessels. The cells showing the most significant increase were mononuclear cells and certain monocyte lines, then CD8+, and finally CD4+ T cells.

Reticulo-endothelial cells were also found to be severely affected within the spleen and lymph nodes.

Injury Due to Inflammatory Damage
The researchers point out that their observations do not correlate with organ damage occurring as a result of a local inflammatory response to the virus since the damage does not occur at all sites of infection nor is it related in time to the occurrence of infection. Instead, the evidence of viral infection is seen in many tissues in fatal COVID-19 for up to 42 days from the earliest symptom.

Again, viral RNA is found in the kidney, liver, and intestine, but there is no sign of injury or inflammation. Thus, viral infection in COVID-19 does not cause localized inflammatory responses. This is true of the presence of the virus in the lung as well. The presence of vasculitis in many cases of COVID-19 was confirmed, but this was not linked to direct viral injury.

 

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There have also been a few studies in the last month suggesting a high percentage of the population have immunity to Sars-CoV-2 via T cells because of previous exposure to other coronaviruses


"Memory T cells induced by previous pathogens can shape the susceptibility to, and clinical severity of, subsequent infections1. Little is known about the presence of pre-existing memory T cells in humans with the potential to recognize SARS-CoV-2. Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in COVID-19 convalescents (n=36). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then showed that SARS-recovered patients (n=23) still possess long-lasting memory T cells reactive to SARS-NP 17 years after the 2003 outbreak, which displayed robust cross-reactivity to SARS-CoV-2 NP. Surprisingly, we also frequently detected SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients (n=37). SARS-CoV-2 T cells in uninfected donors exhibited a different pattern of immunodominance, frequently targeting the ORF-1-coded proteins NSP7 and 13 as well as the NP structural protein. Epitope characterization of NSP7-specific T cells showed recognition of protein fragments with low homology to “common cold” human coronaviruses but conserved amongst animal betacoranaviruses. Thus, infection with betacoronaviruses induces multispecific and long-lasting T cell immunity to the structural protein NP. Understanding how pre-existing NP- and ORF-1-specific T cells present in the general population impact susceptibility and pathogenesis of SARS-CoV-2 infection is of paramount importance for the management of the current COVID-19 pandemic."


SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls

 

And an article published today talking about the as yet undetermined reason T Cells are disappearing in serious covid patients and in that way the disease is behaving like AIDS

The people with hidden immunity against Covid-19

 

It never was the virus

The fatalities are occuring in those that dont have sufficient T cells

Half the fatalities are people that have a BMI over 40, for a 6ft male thats 300lbs

The rest are made up of old people and those that have a suppressed immune response, cancer patients etc

The virus is new, no antibodies, but the rest of us already had a sufficient immune response via T cells

99.7% of us never did have anything to worry about

 

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Cool story bro...

What will you be quoting if you get the virus?

 

Same kind of stuff as the last 391 pages

 

Do you ever actually leave your mom's basement?

 

Its a bad analogy, anyone can die from drowning. Sars-CoV-2, most of us were already immune to it before a vaccine

They are only recent studies, we are at that point of understanding now

 

Were these studies done by "non-experts"?

Because if experts did them we aren't supposed to believe them. Right?

 

These are from people actually studying the virus and the data.

Not from 79 yrs olds that took a cushy government admin job that havent set foot in a lab for 30 years. Fauci, the useless ____

 

Drowning is not the same word as water

 

How long did it take you to figure that out?

Or did you have to look it up first?

 

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