Wuhan Coronavirus - COVID-19 Analysis & Summary - This is not just fucking pneumonia. It is everything but the kitchen sink. Lungs, heart, kidneys, liver, brain, blood vessels, testes. It affects them all.

[derpherp2]

Speaking of coworkers didn't he say one of his coworkers died or some shit on some forum somewhere?

 

[teriyakiburns]

Sauce recipe pls.

Bonus points if you can autistically LARP as OP's spergposting.

I am definitely too drunk for that. If I were to do it, though, I'd link a bunch of BBC goodfoods articles, a biopic of Gordon Ramsey, a couple of episodes of Good Eats, pictures of Guy Fieri, and then claim that non-stick pans aren't real.

1x 800 gram can of chopped tomatoes
approximately 2 to 3 tablespoons of dried oregano
one tablespoonish of dried thyme
a bit less of dried basil
four or five mushrooms
one onion, chopped fine
two sticks of celery, chopped fine
three cloves of garlic, chopped into tiny little bits or pressed into mush
three rashers of lean back bacon, or some sort of italian dried meat if possible, chopped into itty bitty pieces
two or three tablespoons balsamic of modena vinegar
one tablespoon of red wine vinegar
one teaspoon of honey
pepper and salt to taste
olive oil as necessary

blend the tomato and celery until it looks delicious, then put it in a pan on low heat to warm
heat some olive oil in a pan until it starts to smoke
fry the onion until it starts to clear, then throw in the garlic and bacon. fry until the meat is starting to crisp, then throw in the mushroom with a little of the thyme.continue to fry until the oil is gone. add to the pan.
mix all the rest into the pan with the tomato.
bring to the boil, then simmer for about 40 minutes or until it looks tasty.
put on pasta. eat like soup. use as a bread dip. smear it on your naked wife

Works great with tortelloni or pierogis, or that sort of thing, but basically any pasta of any sort. it's about as authentically italian as I am, but it tastes pretty good, and works as a base for any number of explorations. Add a few anchovies for some delicious umami. Add some ground beef for a fairly frisky bolognese. Add more pork to keep the jews and muslims at bay.

Pairs best with nice lisboa (yes I know pairing italian with portugese wine is heresy but I'm the eternal anglo, so sue me). surprisingly good with wholewheat pasta.

I am not a professional chef.

 

[Drain Todger]

Speaking of coworkers didn't he say one of his coworkers died or some shit on some forum somewhere?

Yes. Esther Bryant-Kyles, one of our ticket-takers. It was in the news.

Washington State Ferries: Seattle terminal employee with COVID-19 dies

WSF said the employee had worked for the agency for 25 years.

www.kitsapsun.com

So, yes, as a matter of fact, this thing is already killing our employees.

 

[Yotsubaaa]

You misread that. The first one is plus, the other is a division sign.

@AltisticRight didn't misread, he was making fun of the fact that you fucked up your BEDMAS. There's a reason nobody uses the ÷ division symbol after 5th grade. Which you'd know, if you'd actually gone to a school instead of being home'schooled' by your cultist parents.

We have a word for this attitude. It's called credentialism, and it's a mental disease.

No, credentialism is a fundamental part of how society works. Of course people attach more weight to the words of someone who slogged through years of a postgrad in a relevant field than they do for some guy who has at best a 10th grade education and no formal education in research practice. You sound like a tumblrite.

 

[SIGSEGV]

Yes. Esther Bryant-Kyles, one of our ticket-takers. It was in the news.

Washington State Ferries: Seattle terminal employee with COVID-19 dies

WSF said the employee had worked for the agency for 25 years.

www.kitsapsun.com

So, yes, as a matter of fact, this thing is already killing our employees.

You didn't answer my question, faggot. What's the point of this thread if you aren't going to say anything new? All you're doing is regurgitating shit without even explaining it properly.

 

[derpherp2]

Yes. Esther Bryant-Kyles, one of our ticket-takers. It was in the news.

Not talking to you faggot, but thanks for making it easier. I mean outright saying your area of work while your dox is out is brave and stunning

I'd suggest paying attention to the two people actually debating with you tho, pretty sure there's enough information here.

 

[Yotsubaaa]

I'd suggest paying attention to the two people actually debating with you tho, pretty sure there's enough information here.

I have no expectations that any of us will get through to him at this point. I was watching @Unog thoroughly tear apart all of his points in the chat earlier this morning, and it was all in one ear and out the other with this guy.

EDIT: added link.

 

[Drain Todger]

@AltisticRight didn't misread, he was making fun of the fact that you fucked up your BEDMAS. There's a reason nobody uses the ÷ division symbol after 5th grade. Which you'd know, if you'd actually gone to a school instead of being home'schooled' by your cultist parents.

I copied and pasted that sequence of operations from the calculator in Windows. I didn't use the division symbol intentionally, like hunting through a character map for it.

@AltisticRight No, credentialism is a fundamental part of how society works. Of course people attach more weight to the words of someone who slogged through years of a postgrad in a relevant field than they do for some guy who has at best a 10th grade education and no formal education in research practice. You sound like a tumblrite.

I consulted with experts. Numerous experts. They all agreed my work had merit.

When I mention this, people shift to attacking them and their credibility, or suggesting that their endorsements aren't actually endorsements.

What do people stand to gain by discrediting me? Peace of mind that this virus isn't as bad as I say it is?

Kiwi Farms' stance is not unique. Mind you, I have been banned from three forums and harassed by my coworkers over all this.

And yet, every single scientist that I have contacted has been supportive. Go figure.

 

[SIGSEGV]

I copied and pasted

Oh don't worry, we can tell.

 

[derpherp2]

I copied and pasted that sequence of operations from the calculator in Windows. I didn't use the division symbol intentionally, like hunting through a character map for it.

And again you miss the point

he was making fun of the fact that you fucked up your BEDMAS.

I consulted with experts. Numerous experts. They all agreed my work had merit.

Autistically repeating the same phrase won't make it any more true, faggot.

When I mention this, people shift to attacking them and their credibility, or suggesting that their endorsements aren't actually endorsements.

Yes do you not know how socializing with people works? Especially people that don't believe anything you say?
Of course you don't why am I even asking.

What do people stand to gain by discrediting me? Peace of mind that this virus isn't as bad as I say it is?

Yes yes pity you boohooo boo hoo. Stolen science valour isn't working out for you, waaaaaaaaaah.

Kiwi Farms' stance is not unique. Mind you, I have been banned from three forums and harassed by my coworkers over all this.

Uh huh you're such a badass boohoo boohoo

And yet, every single scientist that I have contacted has been supportive. Go figure.

sure they have buuuuuud. Those two letters you showed us were totally supportive

So when're you actually going to argue their actual points?

 

[It's HK-47]

 

[SIGSEGV]

View attachment 1219791

Hold the fuck up.

Isn't Sweetie Bell a child?

 

[derpherp2]

Hold the fuck up.
View attachment 1219800
Isn't Sweetie Bell a child?

Sweetie Belle is a school-age unicorn pony and Rarity's younger sister.

Dude cmon, you can keep pretending you don't care about this shit but going on mid-jackoff about what you're doing with your life implies either guilt or premature ejaculation sadness.
Considering your rotund weight it could be both.

 

[Horrors of the Deep]

And yet, every single scientist that I have contacted has been supportive. Go figure.

Academics, please respond.

Did we get to nipple clamps yet? Jokes aside train dodger being undercover Kraut would be a gift from the gods and prove that this is the best timeline despite all the shit that's happening.

 

[ADHD]

Hold the fuck up.
View attachment 1219800
Isn't Sweetie Bell a child?

I mean I'm not a pony expert but that sure looks like a child.

 

[Drain Todger]

Hold the fuck up.
View attachment 1219800
Isn't Sweetie Bell a child?

Yeah. Dailevy's Secret Horse Files. That game is disgusting. Wanna try it? The creator has a whole fucking Patreon dedicated to it.

https://www.patreon.com/posts/secret-horse-3-25907472

That is far and away not the most disgusting flash game I've ever played.

That honor belongs to StudioS and their games, which feature nipple torture and candle wax torture, and turned even my iron stomach.

Spoiler: Really, Really NSFW

LewdLook: Ryoujoku Hajigoku

www.lewdgamer.com

Good god. You guys really haven't been around the block with this stuff, have you? Jesus. You're a bunch of choir boys.

You didn't answer my question, faggot. What's the point of this thread if you aren't going to say anything new? All you're doing is regurgitating shit without even explaining it properly.

Well, I would explain it in great detail if you'd just sit down for a second and let me.

ACE2 receptors are found in a wide variety of human cell lines. The virus can attack many cell types, not just those found in the lungs. It can cause multi-organ systemic inflammation and all sorts of issues.

 

[SIGSEGV]

The virus can attack many cell types, not just those found in the lungs. It can cause multi-organ systemic inflammation and all sorts of issues.

Does it actually do any of those things though?

 

[Drain Todger]

Does it actually do any of those things though?

All the evidence I've gathered says yes. This virus provokes a severe host response (i.e. cytokine storm) inside multiple vital organs. I have gathered concrete evidence of this.

Clinical pathology of critical patient with novel coronavirus pneumonia (COVID-19) (2020-02-26) [https://www.preprints.org/manuscript/202002.0407/v3/download]

This PDF contains photo evidence of biopsied lung tissue (from a 66-year-old man in Wuhan who received a double lung transplant and whose condition reportedly improved).

This is what his lungs looked like after they were removed:

Spoiler: Gruesome Lungs

Furthermore, the document describes the histopathological findings.

Masson staining indicated massive pulmonary
interstitial fibrosis. Immunohistochemistry results showed positive for immunity cells
including CD3, CD4, CD8, CD20, CD79a, CD5, CD38 and CD68.

Recent study indicates that SARS-CoV-2 has the same cell entry receptor ACE2 as
SARS-CoV.12,13 Generally, ACE2 protein is expressed in alveolar cells, bronchial
epithelium and vascular endothelium, therefore SARS-CoV-2 protein binds to ACE2
would result in acute lung injury and pulmonary edema. We observed abundant
pulmonary edema and hemorrhage, desquamated bronchial and alveolar epithelial cells.
On the other side, cytokine storm links to an excessively exaggerated immune response,
and uncontrolled proinflammatory responses, which causes severe organ diseases
including lung damages.14-16 Several representative cytokines have been identified
including IL-1β, IL-18, TNF-α, IL-6, IL-8 and IL-10, which are produced and regulated
by various immunological cells including CD8 and CD4 T cells.17 Interestingly, we
observed that lymphocytes, monocytes and plasma cells infiltrating into pulmonary
interstitium, and these types of inflammatory cells were confirmed by immunohistological
method. As we demonstrate above, many pathological changes occurred in pulmonary
interstitium including extensive interstitial fibrosis and vessels lumen stenosis. Therefore,
these results might explain why critical patient had acute lung dysfunction.

Hemorrhagic necrosis of lungs, check. Cytokine storm in lung tissue, check.

Moving on.

Here's another patient, a 50-year-old man who died of COVID-19:

Pathological findings of COVID-19 associated with acute respiratory distress syndrome (2020-02-1 [https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext]

Biopsy samples were taken from lung, liver, and heart tissue of the patient. Histological examination showed bilateral diffuse alveolar damage with cellular fibromyxoid exudates (figure 2A, B). The right lung showed evident desquamation of pneumocytes and hyaline membrane formation, indicating acute respiratory distress syndrome (ARDS; figure 2A). The left lung tissue displayed pulmonary oedema with hyaline membrane formation, suggestive of early-phase ARDS (figure 2B). Interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in both lungs. Multinucleated syncytial cells with atypical enlarged pneumocytes characterised by large nuclei, amphophilic granular cytoplasm, and prominent nucleoli were identified in the intra-alveolar spaces, showing viral cytopathic-like changes. No obvious intranuclear or intracytoplasmic viral inclusions were identified.

...


In addition, the liver biopsy specimens of the patient with COVID-19 showed moderate microvesicular steatosis and mild lobular and portal activity (figure 2C), indicating the injury could have been caused by either SARS-CoV-2 infection or drug-induced liver injury. There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue (figure 2D).
Peripheral blood was prepared for flow cytometric analysis. We found that the counts of peripheral CD4 and CD8 T cells were substantially reduced, while their status was hyperactivated, as evidenced by the high proportions of HLA-DR (CD4 3·47%) and CD38 (CD8 39·4%) double-positive fractions (appendix p 3). Moreover, there was an increased concentration of highly proinflammatory CCR6+ Th17 in CD4 T cells (appendix p 3). Additionally, CD8 T cells were found to harbour high concentrations of cytotoxic granules, in which 31·6% cells were perforin positive, 64·2% cells were granulysin positive, and 30·5% cells were granulysin and perforin double-positive (appendix p 3). Our results imply that overactivation of T cells, manifested by increase of Th17 and high cytotoxicity of CD8 T cells, accounts for, in part, the severe immune injury in this patient.

Telltale signs of cytokine storm in the lungs.

T helper 17 cell - Wikipedia

en.wikipedia.org

Cytotoxic T cell - Wikipedia

en.wikipedia.org

Inflammatory cytokines ripped right through that formerly-healthy lung tissue and destroyed it.

Next, let's see what it does to the rest of the body.

First Case of COVID-19 Infection with Fulminant Myocarditis Complication: Case Report and Insights (2020-03-10) [https://www.preprints.org/manuscript/202003.0180/v1]

Background: The Coronavirus Disease 2019 (COVID-19) has been demonstrated as the cause of pneumonia. Nevertheless, it has not been reported as the cause of acute myocarditis or fulminant myocarditis. Case Presentation: A 63-year-old male was admitted with pneumonia and cardiac symptoms. He was genetically confirmed as COVID-19 by testing sputum on the first day of admission. He also had an elevated troponin-I (Trop I) level and diffuse myocardial dyskinesia along with decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of Interleukin 6 was 272.40pg/ml. Bedside chest radiograph had typical ground-glass changes of viral pneumonia. The laboratory test results of virus that can cause myocarditis are all negative. The patient conformed to the diagnostic criteria of Chinese expert consensus statement for fulminant myocarditis. After receiving antiviral therapy and mechanical life support, the Trop I reduced to 0.10 g/L, and Interleukin 6 was 7.63 pg/ml. Meanwhile the LVEF of the patient gradually recovered to 68%. Conclusion: COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure, and this is the first case of COVID-19 infection complicated with fulminant myocarditis. The mechanism of cardiac pathology caused by COVID-19 needs further study.

Huh, that's strange. It causes heart failure? I thought this was a lung disease. Let's keep looking for more proof of this.

Mysterious Heart Damage, Not Just Lung Troubles, Befalling COVID-19 Patients

Most of the attention in the COVID-19 pandemic has been on how the virus affects the lungs. But evidence shows that up to 1 in 5 hospitalized patients have signs of heart damage and many are dying …

khn.org

In addition to lung damage, many COVID-19 patients are also developing heart problems — and dying of cardiac arrest.

As more data comes in from China and Italy, as well as Washington state and New York, more cardiac experts are coming to believe the COVID-19 virus can infect the heart muscle. An initial study found cardiac damage in as many as 1 in 5 patients, leading to heart failure and death even among those who show no signs of respiratory distress.

That could change the way doctors and hospitals need to think about patients, particularly in the early stages of illness. It also could open up a second front in the battle against the COVID-19 pandemic, with a need for new precautions in people with preexisting heart problems, new demands for equipment and, ultimately, new treatment plans for damaged hearts among those who survive.

Hmm. Oh, maybe I should find one more, just to make sure.

How does COVID-19 affect the heart?

The effects of COVID-19 on the lungs are well-known. As the COVID-19 pandemic continues, more information is becoming available about [...]

newsnetwork.mayoclinic.org

The effects of COVID-19 on the lungs are well-known. As the COVID-19 pandemic continues, more information is becoming available about the role the virus, called SARS-CoV-2, has on the heart. "Individuals with known cardiovascular disease are at an increased risk of more severe complications from respiratory viral illnesses, including the flu and COVID-19," says Dr. Leslie Cooper, chair of the Department of Cardiology at Mayo Clinic.

"We know that during severe SARS-CoV-2 infection, heart function may decrease. Sometimes this decrease is a consequence of the systemic inflammatory response to infection, and occasionally, in some people, because of direct viral infection in the heart."

2 main cardiac issues

According to Dr. Cooper, there are two dominant cardiac issues related to COVID-19: heart failure, when the heart muscle doesn't pump blood as well as it should, and arrhythmias, or abnormal heart rhythms, that can be related to the infection or to the effect of medications used to treat the virus.

Wow, that's interesting. It causes heart failure. I thought this was just pneumonia!

What about the kidneys? Something something, acute kidney injury, something something.

Human Kidney is a Target for Novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection (2020-03-17) [https://www.medrxiv.org/content/10.1101/2020.03.04.20031120v3]

H&E staining demonstrated kidney tissues from postmortems have severe acute tubular necrosis and lymphocyte infiltration. Immunohistochemistry showed that SARS-CoV-2 NP antigen was accumulated in kidney tubules. Viral infection not only induces CD68+ macrophages infiltrated into tubulointerstitium, but also enhances complement C5b-9 deposition on tubules. CONCLUSIONS SARS-CoV-2 induces ARF in COVID-19 patients. Viruses directly infect human kidney tubules to induce acute tubular damage. The viruses not only have direct cytotoxicity, but also initiate CD68+ macrophage together with complement C5b-9 deposition to mediate tubular pathogenesis.

What's that? The virus can directly infect the kidneys and cause renal tubular damage? Maybe I should find one more paper, just to be sure.

Identification of a potential mechanism of acute kidney injury during the COVID-19 outbreak: a study based on single-cell transcriptome analysis (2020-03-31) [https://link.springer.com/article/10.1007/s00134-020-06026-1]

Second, although there was no significant difference in the expression of TMPRSS genes, the expression of the receptor ACE2 in podocytes and proximal straight tubule cells in Occidental donors was more pronounced than that in Asian donors (Fig. S2B), suggesting that Occidental populations might be at higher risk for developing AKI in COVID-19. In addition, comparative analysis showed that the coexpression of the receptor ACE2 and TMPRSS genes in kidney cells was no less than that in the lung, oesophagus, small intestine and colon (Fig. S2C), suggesting that the kidney might also be an important target organ for SARS-CoV-2.
Finally, our study clearly identified podocytes and proximal straight tubule cells as kidney host cells. Podocytes and proximal straight tubule cells play critical roles in urine filtration, reabsorption and excretion. Notably, podocytes are particularly vulnerable to viral and bacterial attacks, and podocyte injury easily induces heavy proteinuria [5]. As recent research data showed, 43.9% of SARS-CoV-2-infected patients, especially those with AKI, had proteinuria [6]. Moreover, a recent study reported the detection of SARS-CoV-2 infection in urine samples of patients with severe COVID-19 [3]. Furthermore, the entry of SARS-CoV-2 into the systemic circulation is also a key process that leads to AKI. According to published data, the length of time between the detection of SARS-CoV-2 in blood samples and AKI occurrence was approximately 7 days [1].
Based on our findings, we conclude that the cytopathic effects of SARS-CoV-2 on podocytes and proximal straight tubule cells may cause AKI in patients with COVID-19, especially in patients with SARS-CoV-2 infection in blood samples. Therefore, we need to pay more attention to the early monitoring of renal function and cautiously handle the urine of COVID-19 patients with AKI to prevent accidental infection. However, our findings were based on an analysis of normal kidney cells: the proposed mechanism of the pathophysiology of AKI during COVID-19 still needs to be validated in autopsy tissues from COVID-19 patients and functional experiments in animals and cells.

Huh, so it can cause renal tubular damage.

There is a contradicting study, however:

Coronavirus Disease 19 Infection Does Not Result in Acute Kidney Injury: An Analysis of 116 Hospitalized Patients from Wuhan, China (2020-03-24) [https://www.karger.com/Article/FullText/507471]

Maybe it doesn't harm the kidneys. We're not quite sure.

What about the liver?

Patients with COVID-19 may face risk for liver injury (2020-03-19) [https://www.the-hospitalist.org/hospitalist/article/219309/coronavirus-updates/patients-covid-19-may-face-risk-liver-injury]

Patients with COVID-19 may be at risk for liver injury, but mechanisms of damage remain unclear, according to investigators.

Proposed mechanisms include direct virus-induced effects, immune-induced damage due to excessive inflammatory responses, and drug-induced injury, reported lead author Ling Xu of Huazhong University of Science and Technology, Wuhan, China, and colleagues.

“From a clinical perspective, in addition to actively dealing with the primary disease caused by coronavirus infection, attention should also be paid to monitor the occurrence of liver injury, and to the application of drugs which may induce liver damage,” the investigators wrote in Liver International. “Patients with liver damage are advised to be treated with drugs that could both protect liver functions and inhibit inflammatory responses, such as ammonium glycyrrhizinate, which may, in turn, accelerate the process of disease recovery.”

Hmm, this is interesting. Apparently, it causes a mild hepatitis.

COVID-19 and the liver: little cause for concern (2020-03-20) [https://www.thelancet.com/journals/langas/article/PIIS2468-1253(20)30084-4/fulltext]

It has been proposed that COVID-19 causes direct liver injury via a viral hepatitis, but we believe that there are alternative explanations. First, the derangement of liver function is clearly mild. Second, when liver function tests for patients with different durations of symptoms are examined, there is no evidence that later presentation is associated with greater liver function derangement.
3
The only post-mortem liver biopsy from a patient with COVID-19 showed only microvesicular steatosis, a common finding in sepsis.
4
Most importantly, other respiratory viruses produce similar elevations of liver function biomarkers, which is thought to relate to hepatic damage from immune interactions involving intrahepatic cytotoxic T cells and Kupffer cells.
5
This phenomenon waxes and wanes in parallel with respiratory viral disease and in the absence of hepatic viral replication, which might explain why worse outcomes were not seen in the 42 patients with chronic liver disease and COVID-19 who had outcome data (table).
Hepatic dysfunction in severe COVID-19 is accompanied by greater activation of coagulative and fibrinolytic pathways, relatively depressed platelet counts, climbing neutrophil counts and neutrophil to lymphocyte ratios, and high ferritin levels.
6
Although these markers are seen as non-specific markers of inflammation, we believe that they fit the paradigm of disease severity coinciding with a failure of innate immune regulation.
7
Such unbalanced immunity favours NETosis and coagulation activation and possibly also alters systemic iron metabolism secondary to macrophage activation.
8
Notably, this alteration of immune balance occurs with increased age, and older patients might therefore be expected to fare worse, with a greater reliance on this pathway.
9

Apparently, this is only really of any concern if someone has pre-existing liver issues, or they're taking drugs that harm the liver. The liver pathology is not severe.

What about the brain?

The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients (2020-02-24) [https://onlinelibrary.wiley.com/doi/pdf/10.1002/jmv.25728]

Following the severe acute respiratory syndrome coronavirus (SARS‐CoV) and Middle East respiratory syndrome coronavirus (MERS‐CoV), another highly pathogenic coronavirus named SARS‐CoV‐2 (previously known as 2019‐nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS‐CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID‐19) with clinical symptoms similar to those reported for SARS‐CoV and MERS‐CoV. The most characteristic symptom of patients with COVID‐19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID‐19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS‐CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse‐connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS‐CoV and SARS‐CoV2, it remains to make clear whether the potential invasion of SARS‐CoV2 is partially responsible for the acute respiratory failure of patients with COVID‐19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS‐CoV‐2‐induced respiratory failure.

So, it can get into the medulla through the parasympathetic nerves of the lung and then the vagus nerve? It's neurotropic?

Hmm, I wonder if any other documents support this finding?

Neurological Manifestations of Hospitalized Patients with COVID-19 in Wuhan, China: a retrospective case series study (2020-02-25) [https://www.medrxiv.org/content/10.1101/2020.02.22.20026500v1]

Coronaviruses can cause multiple systemic infections or injuries in various animals [5]. However, some of them can adapt fast and cross the species barrier, such as in the cases of SARS-CoV and Middle East respiratory syndrome-CoV (MERS-CoV), causing epidemics or pandemics. Infection in human often leads to severe clinical symptoms and high mortality [6]. As for COVID-19, several studies have described clinical manifestations including respiratory symptoms, myalgia and fatigue. COVID-19 also has characteristic laboratory findings and lung CT abnormalities [7]. However, it has not been reported that patients with COVID-19 had any neurological manifestations. Here, we would like to report the characteristic neurological manifestation of SARSCoV-2 infection in 78 of 214 patients with laboratory-confirmed diagnosis of COVID-19 and treated at our hospitals, which are located in the epicenter of Wuhan.

...

Recently, ACE2 is identified as the functional receptor for SARS-CoV-2 [3], which is present in multiple human organs, including nervous system and skeletal muscle [11]. The expression and distribution of ACE2 remind us that the SARS-CoV-2 may cause some neurological symptoms through direct or indirect mechanisms. Neurological injury has been confirmed in the infection of other coronavirus such as in SARS-CoV and MERS-CoV. The researchers detected SARS-CoV nucleic acid in the cerebrospinal fluid of those patients and also in their brain tissue on autopsy [12- 13]. CNS symptoms were the main form of neurological injury in patients with COVID19 in this study. The pathological mechanism may be from the CNS invasion of SARS-CoV-2, similar to SARS and MERS virus. Like other respiratory viruses, SARS-COV-2 may enter the CNS through the hematogenous or retrograde neuronal route. The latter can be supported by the fact that some patients in this study had hyposmia. We also found that the lymphocyte counts were lower for patients with CNS symptoms than without CNS symptoms. This phenomenon may be indicative of the immunosuppression in COVID-19 patients with CNS symptoms, especially in the severe subgroup. Moreover, we found severe patients had higher D-dimer levels than that of non-severe patients. This may be the reason why severe patients are more likely to develop cerebrovascular disease. Consistent with the previous studies [7] muscle symptom was also common in our study. We speculate that the symptom was due to skeletal muscle injury, as confirmed by elevated creatine kinase levels. We found that patients with muscle symptoms had higher creatine kinase and lactate dehydrogenase levels than those without muscle symptoms. Furthermore, creatine kinase and lactate dehydrogenase levels in severe patients were much higher than those of none-severe patients. This injure could be related to ACE2 in skeletal muscle [14]. However, SARS-CoV, using the same receptor, was not detected in skeletal muscle by post-mortem examination [15]. Therefore, whether SARS-CoV-2 infects skeletal muscle cells by binding with ACE2 requires to be further studied. One other reason was the infection-mediated harmful immune response that caused the nervous system abnormalities. Significantly elevated pro-inflammatory cytokines in serum may cause muscle damage. This study has several limitations. First, only 214 patients were studied, which could cause biases in clinical observation. It would be better to include more patients from Wuhan, other cities in China, and even other countries. Second, all data were abstracted from the electronic medical records, certain patients with neurological problem might not be captured if their neurological symptoms were too mild, such as with hypogeusia and hyposmia . Third, because most patients were still hospitalized and information regarding clinical outcomes was unavailable at the time of analysis, it was difficult to assess the effect of these neurologic manifestations on their outcome, and continued observations of the natural history of disease are needed.

So, like SARS and MERS, it can invade the central nervous system. Severe patients had higher D-dimer levels (and probably more blood clots) than non-severe patients. The virus can potentially harm skeletal muscle and put muscle breakdown products into the blood. Patients had also lost their sense of taste (hypogeusia) and smell (hyposmia).

Hmm, what else?

Beijing hospital confirms nervous system infections by novel coronavirus (2020-03-05) [http://www.xinhuanet.com/english/2020-03/05/c_138846529.htm]

Previous studies show that COVID-19 may attack multiple organs, including kidneys, livers and heart, but there are no records about the central nervous system damage.

The patient, 56, was diagnosed with the COVID-19 on Jan. 24 at the hospital. He had severe symptoms and failed to respond to regular treatment, according to a hospital statement.

In the intensive care unit (ICU), the patient developed symptoms associated with decreased consciousness, though there were no abnormal signs on his head CT images.

The medical staff then conducted gene sequencing on samples of his cerebrospinal fluid and confirmed the presence of the novel coronavirus, diagnosing the COVID-19 patient with encephalitis, an inflammation of the brain.

He had the virus in his cerebrospinal fluid? Encephalitis? Well, it's definitely in the brain.

Hmm, let's see.

https://pubs.rsna.org/doi/10.1148/radiol.2020201187

Acute necrotizing encephalopathy (ANE) is a rare complication of influenza and other viral infections and has been related to intracranial cytokine storms, which result in blood-brain-barrier breakdown, but without direct viral invasion or parainfectious demyelination (3). Accumulating evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome (4). While predominantly described in the pediatric population, ANE is known to occur in adults as well. The most characteristic imaging feature includes symmetric, multifocal lesions with invariable thalamic involvement (5). Other commonly involved locations include the brain stem, cerebral white matter, and cerebellum (5). Lesions appear hypoattenuating on CT images and MRI demonstrates T2 FLAIR hyperintense signal with internal hemorrhage. Postcontrast images may demonstrate a ring of contrast enhancement (5).

Wow, this patient had a cytokine storm in her brain that did the same thing to her brain tissue that excess cytokines did to that 66-year-old patient's lungs.

Oh! What's this? My buddy on Twitter, Farid Jalali, MD, who I talked with over DM, had this to offer:

http://farid.jalali.one/covid19emailpdf.pdf?fbclid=IwAR3eTVxEDcZdRHl99pd0-zHgqLzmirMz1v7pnnJa-Dz25oWFPu4j5_IAkMw

1) Possible reason for ACE inhibitor use as risk for severe COVID-19, due to, 2) MICROVASCULAR THROMBOSIS as the unifying fatal insult in severe COVID-19, due to progressive SEVERE ENDOTHELIAL DYSFUNCTION

So, basically, to sum up, COVID-19 causes cytokine storms and severe inflammation and tissue damage in many of major organs, hypoxemia, and diffuse clotting.

And doctors can't figure out why patients on ventilators are dying.

Hint, it's because their capillaries can no longer exchange oxygen with their alveoli.

It's not a "lung disease".

COVID-19 is a blood and vascular disease that ninja-attacks all your major fucking organs while also giving you insane inflammatory damage.

The ventilator settings most doctors are using will do approximately something between jack and shit, and they are confused as fuck:

 

[Jan_Hus]

All the evidence I've gathered says yes. This virus provokes a severe host response (i.e. cytokine storm) inside multiple vital organs. I have gathered concrete evidence of this.

Clinical pathology of critical patient with novel coronavirus pneumonia (COVID-19) (2020-02-26) [https://www.preprints.org/manuscript/202002.0407/v3/download]

This PDF contains photo evidence of biopsied lung tissue (from a 66-year-old man in Wuhan who received a double lung transplant and whose condition reportedly improved).

This is what his lungs looked like after they were removed:

Spoiler: Gruesome Lungs

Furthermore, the document describes the histopathological findings.





Hemorrhagic necrosis of lungs, check. Cytokine storm in lung tissue, check.

Moving on.

Here's another patient, a 50-year-old man who died of COVID-19:

Pathological findings of COVID-19 associated with acute respiratory distress syndrome (2020-02-1 [https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext]



Telltale signs of cytokine storm in the lungs.

T helper 17 cell - Wikipedia

en.wikipedia.org

Cytotoxic T cell - Wikipedia

en.wikipedia.org

Inflammatory cytokines ripped right through that formerly-healthy lung tissue and destroyed it.

Next, let's see what it does to the rest of the body.

First Case of COVID-19 Infection with Fulminant Myocarditis Complication: Case Report and Insights (2020-03-10) [https://www.preprints.org/manuscript/202003.0180/v1]



Huh, that's strange. It causes heart failure? I thought this was a lung disease. Let's keep looking for more proof of this.

Mysterious Heart Damage, Not Just Lung Troubles, Befalling COVID-19 Patients

Most of the attention in the COVID-19 pandemic has been on how the virus affects the lungs. But evidence shows that up to 1 in 5 hospitalized patients have signs of heart damage and many are dying …

khn.org

Hmm. Oh, maybe I should find one more, just to make sure.

How does COVID-19 affect the heart?

The effects of COVID-19 on the lungs are well-known. As the COVID-19 pandemic continues, more information is becoming available about [...]

newsnetwork.mayoclinic.org

Wow, that's interesting. It causes heart failure. I thought this was just pneumonia!

What about the kidneys? Something something, acute kidney injury, something something.

Human Kidney is a Target for Novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection (2020-03-17) [https://www.medrxiv.org/content/10.1101/2020.03.04.20031120v3]



What's that? The virus can directly infect the kidneys and cause renal tubular damage? Maybe I should find one more paper, just to be sure.

Identification of a potential mechanism of acute kidney injury during the COVID-19 outbreak: a study based on single-cell transcriptome analysis (2020-03-31) [https://link.springer.com/article/10.1007/s00134-020-06026-1]



Huh, so it can cause renal tubular damage.

There is a contradicting study, however:

Coronavirus Disease 19 Infection Does Not Result in Acute Kidney Injury: An Analysis of 116 Hospitalized Patients from Wuhan, China (2020-03-24) [https://www.karger.com/Article/FullText/507471]

Maybe it doesn't harm the kidneys. We're not quite sure.

What about the liver?

Patients with COVID-19 may face risk for liver injury (2020-03-19) [https://www.the-hospitalist.org/hospitalist/article/219309/coronavirus-updates/patients-covid-19-may-face-risk-liver-injury]



Hmm, this is interesting. Apparently, it causes a mild hepatitis.

COVID-19 and the liver: little cause for concern (2020-03-20) [https://www.thelancet.com/journals/langas/article/PIIS2468-1253(20)30084-4/fulltext]



Apparently, this is only really of any concern if someone has pre-existing liver issues, or they're taking drugs that harm the liver. The liver pathology is not severe.

What about the brain?

The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients (2020-02-24) [https://onlinelibrary.wiley.com/doi/pdf/10.1002/jmv.25728]



So, it can get into the medulla through the parasympathetic nerves of the lung and then the vagus nerve? It's neurotropic?

Hmm, I wonder if any other documents support this finding?

Neurological Manifestations of Hospitalized Patients with COVID-19 in Wuhan, China: a retrospective case series study (2020-02-25) [https://www.medrxiv.org/content/10.1101/2020.02.22.20026500v1]



So, like SARS and MERS, it can invade the central nervous system. Severe patients had higher D-dimer levels (and probably more blood clots) than non-severe patients. The virus can potentially harm skeletal muscle and put muscle breakdown products into the blood. Patients had also lost their sense of taste (hypogeusia) and smell (hyposmia).

Hmm, what else?

Beijing hospital confirms nervous system infections by novel coronavirus (2020-03-05) [http://www.xinhuanet.com/english/2020-03/05/c_138846529.htm]



He had the virus in his cerebrospinal fluid? Encephalitis? Well, it's definitely in the brain.

Hmm, let's see.

https://pubs.rsna.org/doi/10.1148/radiol.2020201187

Wow, this patient had a cytokine storm in her brain that did the same thing to her brain tissue that excess cytokines did to that 66-year-old patient's lungs.

Oh! What's this? My buddy on Twitter, Farid Jalali, MD, who I talked with over DM, had this to offer:

http://farid.jalali.one/covid19emailpdf.pdf?fbclid=IwAR3eTVxEDcZdRHl99pd0-zHgqLzmirMz1v7pnnJa-Dz25oWFPu4j5_IAkMw

So, basically, to sum up, COVID-19 causes cytokine storms and severe inflammation and tissue damage in many of major organs, hypoxemia, and diffuse clotting.

And doctors can't figure out why patients on ventilators are dying.

Hint, it's because their capillaries can no longer exchange oxygen with their alveoli.

It's not a "lung disease".

COVID-19 is a blood and vascular disease that ninja-attacks all your major fucking organs while also giving you insane inflammatory damage.

The ventilator settings most doctors are using will do approximately something between jack and shit, and they are confused as fuck:

You do realize that the flu can do all of this as well right?

 

[Drain Todger]

You do realize that the flu can do all of this as well right?

Yeah, sure. Getting run over by a car can flatten you. So can getting run over by a train.

The flu is the car. COVID-19 is the locomotive.