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.

evrae said:
I'll look at responses to my posts in particular to be a bit more brief.

The paper you linked is on medrxiv, this is essentially a pre-print archive, this means it isn't peer-reviewed yet. This isn't necessarily a bad thing, all papers go through pre-print, but this means you should be more cautious about them.

Looking at the paper itself it states within the Findings section near the start that NAbs and spike-binding antibodies were significantly higher in elderly patients and the middle-aged compared to young patients. This paper states this may be as the result of a strong immune response within older patients but it's not sure if this actually has a role in preventing progression into worse states. It also states it couldn't get samples from patients in severe or critical conditions as they received passive antibody treatment before sample collection (would heavily bias samples from these patients). It seems like in patients that can rapidly clear CoV-2 the immune system doesn't particularly bother with NAbs, the paper also states that other immune responses (including T cells or cytokines) may have contributed to the recovery of patients with below detectable levels. The paper also states that the potential of rebound or reinfection should be investigated in further studies, suggesting that this hasn't even been confirmed and that the gun shouldn't be jumped in this regard (which is something you're actually doing, in this case).
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Yes. Yes, exactly! There is a possibility that people are still testing positive after the fact because they have latent virus that hasn't been cleared, not because they've actually been "reinfected", of course. Some people who were infected with Ebola had detectable virus in their bodies months and months later.

I think there's some confusion over this "reinfection" business. It needs a lot more study, I agree.

evrae said:
With regards to steroid use, I wasn't aware of China's extensive use of them in their treatments. For the concern over suppressing the immune system too hard, this is what doctors are trained for, drugs have what is called the therapeutic window in which below that it does nothing noticeable and above that toxic effects occur. This of course would be used in combination with other treatments available that will help handle the virus itself which should help lessen the risk of any sort of effects caused by trying to dampen the immune system.
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Yep, they used steroids extensively. And TCM. Except Traditional Chinese Medicine is complete nonsense and no amount of bear bile or ground-up rhino horn can help with this virus.


We identified 24 clinical trials, involving more than 20 medicines, such as human immunoglobulin, interferons, chloroquine, hydroxychloroquine, arbidol, remdesivir, favipiravir, lopinavir, ritonavir, oseltamivir, methylprednisolone, bevacizumab, and traditional Chinese medicines (TCM). Although drug repurposing has some limitations, repositioning clinical trials may represent an attractive strategy because they facilitate the discovery of new classes of medicines; they have lower costs and take less time to reach the market; and there are existing pharmaceutical supply chains for formulation and distribution.
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Methylpred was used extensively in the first SARS outbreak, too. It had severe long-term consequences for some of the patients. They developed osteonecrosis of the joints.


Of the 114 patients, 43 (37.7%) were found to have osteonecrosis. A total of 145 ARCO stage-I osteonecrotic lesions were detected by T1-weighted coronal imaging. The distribution of the lesions is shown in Figure 1. Of the 43 affected patients, 30 (69.8%) had only one or two areas of osteonecrosis and in these, involvement of the joints was the most common presentation, 53 of the 57 sites being epiphyseal and four diaphyseal (Fig. 2). The other 13 patients (30.2%) had multifocal osteonecrosis affecting between three and seven sites. In this group there were 65 epiphyseal lesions, principally involving the hip, knees and shoulders, and 23 diaphyseal lesions (Fig. 2). Diaphyseal lesions occurred in patients with multifocal osteonecrosis more commonly than in those with uni- or bifocal osteonecrosis (Fisher’s exact two-sided test, p = 0.004).

Intravenous methylprednisolone (40 mg/day to 980 mg/ day) and oral prednisone (2.5 mg/day to 20 mg/day) had been administered to all patients within a mean period of 28.2 days (6 to 72). It was initially given to those who were deteriorating and was stopped when they began to recover. The mean time interval between starting steroid therapy and follow-up was 6.5 months (5 to 8).

Logistic regression analysis showed that the peak methylprednisolone-equivalent dose was the principal risk factor for uni- or bifocal osteonecrosis (p < 0.05). No risk factor was found to be associated with multifocal osteonecrosis.
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My own father has a drug-induced injury. He had a sinus operation and took Levaquin (Levofloxacin, a dangerous fluoroquinolone antibiotic that eventually got a black-box warning from the FDA) to clear up the infection, and you know what? It fucked up his tendons in his shoulders and gave him numbness and paresthesia in his feet. Permanent damage. He should've sued Johnson & Johnson.

God. These poor people. :(

evrae said:
The loss of T Lymphocytes would be of course due to the immune system targeting infected T cells which is something I described as what happens, this could be treated with the antiviral side of drugs, which would target things such as the Spike protein. This would help prevent cell entry (or reduce viral load in some other way) and as a result would reduce the number of cells being flagged as infected.
I should have mentioned the elevation of other pro-inflammatory cytokines, but I assumed it was fairly obvious.
Click to expand...

Yep. Exactly. To sum up what I was saying earlier, these people infected with COVID-19 (the ones with clinical-level symptoms, not the sub-clinical, asymptomatic infections, of course; I don't mean to say that everyone develops these complications, they're actually somewhat rare) have variously developed silent hypoxemia, severe bilateral viral pneumonia and ARDS, myocarditis and pericarditis (with notable arrhythmia), hypokalemia, elevated ferritin, lymphopenia (viral T cell attack), thrombocytopenia (platelets are used up by disseminated coagulation), elevated D-dimer, mild hepatitis (indicated by abnormal AST/ALT levels), possible renal tubular damage, possible damage to the seminiferous ducts and male fertility, possible GI tract involvement, and also, potential neurotropism and viral invasion of the cardiorespiratory center of the medulla, in addition to causing cytokine storms wherever it sets up a site of infection.

The virus uses up ACE2 receptors and prevents the degradation of Angiotensin II, and then, the excess Ang II activates AT1R receptors and has a pro-inflammatory, vasoconstrictive effect.

I was worried that this abnormal hormone buildup may be causing focal vasoconstriction in the alveoli, leading to hypoxemia and starving the organs of oxygen. Another possibility that has been raised is disseminated intravascular coagulation causing clotting that blocks off the capillaries, essentially causing little infarcts everywhere. Some of these people infected with this virus have highly elevated D-dimer levels. Like 1500+. They're clotting all over the place, and then, they suffer heart attacks and die.

I was seeing people on 4chan saying "LOL, this person died of a heart attack and they're counting it as a COVID-19 death! They're lying!"

These people don't understand that COVID-19 causes heart attacks.

evrae said:
Vasoconstriction caused by angiotensin 2 can be dealt with by vasodilator drugs, or if you want to be more specific you can use angiotensin 2 receptor blockers.
I have mentioned previously that MERS and other SARS viruses are capable of avoiding immunosurveillance in this way too I believe.

You'd likely be looking at combination therapy with an antiviral (to target the virus), a drug that keeps inflammation in check (for obvious reasons) and possibly a vasodilator/ARB to rectify overt vasoconstriction. The excess vasoconstriction is possibly the reason why risk factors such as hypertension and CVD are some of the bigger risk factors in terms of danger.
Click to expand...

At first, they were worried ARBs might have a negative effect. Now, research is emerging that they may have a beneficial effect, which is good news.

There's conflicting data on this. It's an interesting point:

Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia (2020-02-16) [https://www.ncbi.nlm.nih.gov/pubmed/32061198]

ACE inhibitors and angiotensin receptor blockers may increase the risk of severe COVID-19, paper suggests (2020-03-23) [https://www.sciencedaily.com/releases/2020/03/200323101354.htm]

But you see what I'm saying, right?

Come on. I've been getting my ass handed to me, here, @evrae

Very few people understand the biomed terminology, but you do. What do you think? Do I have a point in all this?

Spooky Bones said:
He genuinely thinks he's some polymath because mom & dad praised his initiative in getting into those sporadic intense interests that autistic children have. He never grew out of it unfortunately.
Click to expand...

This thread has helped me identify some serious holes in my knowledge base.

I think, on the whole, it has been a productive encounter.

ShinyStar said:
If you ever worked at DARPA, you would have a totally different set of priorities based on the fact that you would have had to actually learn something in order to get there. You aren't ever going to work at DARPA because you're lazy and stupid, so any scenario that would put you in a position to be enacting your current idiotic opinions is about as realistic as me prattling on about what I'd do if magic were a thing and I were head-wizard at Hogwarts.
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Well, shit. Now I guess I'm gonna have to do it. I guess I'm gonna have to work on my education, go to college, and just go fucking do it.

I'm so fucking bored. I wanna create fancy toys and blow shit up on the taxpayer's dime. Come on. Wouldn't you want to? Wouldn't you do it if you had the chance?

Look at those guys shooting that prototype railgun on the range at NSWC Dahlgren. They wake up to the smell of ozone and molten metal.


They're living the fucking dream, while I'm just lubricating boats and licking doorknobs. Fuck.

Ped Xing said:
What's ridiculous is you think you're qualified to talk about infantry combat loads when you couldn't even lift an M2 receiver.
Click to expand...

My last day of work, I lifted a Class 150 bronze check valve with a 6" flange right off the deck. Those weigh about twice as much as an M2 receiver, like 130 fucking pounds. I lifted it and walked it several feet so we could get it up a flight of stairs. The guy I was working with, his eyes got wide and he was like "holy shit".

I do shit like shooting .308 rifles one-handed like pistols, for fun. This idea that I can't lift is ridiculous. I have plenty of muscle.

Here, for a laugh, watch my fat ass make a fool of myself and brass myself in the face with my .50 AE Deagle, leaving a perfect Hornady headstamp mark stamped right on my forehead.


I don't know why it's doing that. I don't think I'm limp-wristing it. It just seems to be ejecting right over the top of the slide for some reason. I think I need to take apart the bolt and replace the extractor and ejector springs.

The AR pistols have Kentri short buffers from Pantheon Arms. Those are kinda silly because you have to unscrew the end cap of the buffer tube and pull the guts out to pivot open the action, otherwise, you can't open it to clean it.

www.pantheonarms.com

Kentri Short Buffer System - SB Tactical | Pantheon Arms

The product has been discontinued. Replacement springs will continue to be available. With the Kentri short buffer system you make your AR rifle or pistol more compact, and still have the option to use a pistol stabilizing brace, without breaking the bank. Made from type III hardcoat anodized...
www.pantheonarms.com www.pantheonarms.com
 
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Oh shit, finally some good fucking autism. Drain Tarder, why are you so fat? You sperg in response to everything but only give a one-sentence response to someone asking if you’re going to lose weight. You realize most of the severe cases in young people are in obese individuals because being fat fucks up your immune function, to the point where it’s comparable to someone 20+ years older? You seem to want to cherry pick case studies where the virus is especially severe to rile up the idea that we need to take this more seriously. What you should be doing Pubmed searches on how your Mountain Dew and Cheetos habits are going to fuck you over much harder than a virus will and then make some life changes. But I guess it’s easier to sit there and do nothing about a health problem in your control while obessing over one that’s not.

Also are you a trans-identified individual, or is this just an online persona? Would you describe your relationship with your dad as co-dependent? Did you give in to his pressure to not move out because you’re actually desperately lonely, always online and have no friends, so you cling to the only real human contact you can get?
 
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Ped Xing said:
He did kiss Kristen Johnston when she was payed to let him do that.

Have you ever paid anyone to kiss you?
Click to expand...

No comment.

Seriously, though, who doesn't love Wayne Knight?


BIG DADDY said:
Oh shit, finally some good fucking autism. Drain Tarder, why are you so fat? You sperg in response to everything but only give a one-sentence response to someone asking if you’re going to lose weight. You realize most of the severe cases in young people are in obese individuals because being fat fucks up your immune function, to the point where it’s comparable to someone 20+ years older? You seem to want to cherry pick case studies where the virus is especially severe to rile up the idea that we need to take this more seriously. What you should be doing Pubmed searches on how your Mountain Dew and Cheetos habits are going to fuck you over much harder than a virus will and then make some life changes. But I guess it’s easier to sit there and do nothing about a health problem in your control while obessing over one that’s not.

Also are you a trans-identified individual, or is this just an online persona? Would you describe your relationship with your dad as co-dependent? Did you give in to his pressure to not move out because you’re actually desperately lonely, always online and have no friends, so you cling to the only real human contact you can get?
Click to expand...

 
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Drain Todger said:
Yes. Yes, exactly! There is a possibility that people are still testing positive after the fact because they have latent virus that hasn't been cleared, not because they've actually been "reinfected", of course. Some people who were infected with Ebola had detectable virus in their bodies months and months later.

I think there's some confusion over this "reinfection" business. It needs a lot more study, I agree.



Yep, they used steroids extensively. And TCM. Except Traditional Chinese Medicine is complete nonsense and no amount of bear bile or ground-up rhino horn can help with this virus.




Methylpred was used extensively in the first SARS outbreak, too. It had severe long-term consequences for some of the patients. They developed osteonecrosis of the joints.




My own father has a drug-induced injury. He had a sinus operation and took Levaquin (Levofloxacin, a dangerous fluoroquinolone antibiotic that eventually got a black-box warning from the FDA) to clear up the infection, and you know what? It fucked up his tendons in his shoulders and gave him numbness and paresthesia in his feet. Permanent damage. He should've sued Johnson & Johnson.

God. These poor people. :(



Yep. Exactly. To sum up what I was saying earlier, these people infected with COVID-19 (the ones with clinical-level symptoms, not the sub-clinical, asymptomatic infections, of course; I don't mean to say that everyone develops these complications, they're actually somewhat rare) have variously developed silent hypoxemia, severe bilateral viral pneumonia and ARDS, myocarditis and pericarditis (with notable arrhythmia), hypokalemia, elevated ferritin, lymphopenia (viral T cell attack), thrombocytopenia (platelets are used up by disseminated coagulation), elevated D-dimer, mild hepatitis (indicated by abnormal AST/ALT levels), possible renal tubular damage, possible damage to the seminiferous ducts and male fertility, possible GI tract involvement, and also, potential neurotropism and viral invasion of the cardiorespiratory center of the medulla, in addition to causing cytokine storms wherever it sets up a site of infection.

The virus uses up ACE2 receptors and prevents the degradation of Angiotensin II, and then, the excess Ang II activates AT1R receptors and has a pro-inflammatory, vasoconstrictive effect.

I was worried that this abnormal hormone buildup may be causing focal vasoconstriction in the alveoli, leading to hypoxemia and starving the organs of oxygen. Another possibility that has been raised is disseminated intravascular coagulation causing clotting that blocks off the capillaries, essentially causing little infarcts everywhere. Some of these people infected with this virus have highly elevated D-dimer levels. Like 1500+. They're clotting all over the place, and then, they suffer heart attacks and die.

I was seeing people on 4chan saying "LOL, this person died of a heart attack and they're counting it as a COVID-19 death! They're lying!"

These people don't understand that COVID-19 causes heart attacks.



At first, they were worried ARBs might have a negative effect. Now, research is emerging that they may have a beneficial effect, which is good news.

There's conflicting data on this. It's an interesting point:

Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia (2020-02-16) [https://www.ncbi.nlm.nih.gov/pubmed/32061198]

ACE inhibitors and angiotensin receptor blockers may increase the risk of severe COVID-19, paper suggests (2020-03-23) [https://www.sciencedaily.com/releases/2020/03/200323101354.htm]

But you see what I'm saying, right?

Come on. I've been getting my ass handed to me, here, @evrae

Very few people understand the biomed terminology, but you do. What do you think? Do I have a point in all this?



This thread has helped me identify some serious holes in my knowledge base.

I think, on the whole, it has been a productive encounter.



Well, shit. Now I guess I'm gonna have to do it. I guess I'm gonna have to work on my education, go to college, and just go fucking do it.

I'm so fucking bored. I wanna create fancy toys and blow shit up on the taxpayer's dime. Come on. Wouldn't you want to? Wouldn't you do it if you had the chance?

Look at those guys shooting that prototype railgun on the range at NSWC Dahlgren. They wake up to the smell of ozone and molten metal.


They're living the fucking dream, while I'm just lubricating boats and licking doorknobs. Fuck.



My last day of work, I lifted a Class 150 bronze check valve with a 6" flange right off the deck. Those weigh about twice as much as an M2 receiver, like 130 fucking pounds. I lifted it and walked it several feet so we could get it up a flight of stairs. The guy I was working with, his eyes got wide and he was like "holy shit".

I do shit like shooting .308 rifles one-handed like pistols, for fun. This idea that I can't lift is ridiculous. I have plenty of muscle.

Here, for a laugh, watch my fat ass make a fool of myself and brass myself in the face with my .50 AE Deagle, leaving a perfect Hornady headstamp mark stamped right on my forehead.


I don't know why it's doing that. I don't think I'm limp-wristing it. It just seems to be ejecting right over the top of the slide for some reason. I think I need to take apart the bolt and replace the extractor and ejector springs.

The AR pistols have Kentri short buffers from Pantheon Arms. Those are kinda silly because you have to unscrew the end cap of the buffer tube and pull the guts out to pivot open the action, otherwise, you can't open it to clean it.

www.pantheonarms.com

Kentri Short Buffer System - SB Tactical | Pantheon Arms

The product has been discontinued. Replacement springs will continue to be available. With the Kentri short buffer system you make your AR rifle or pistol more compact, and still have the option to use a pistol stabilizing brace, without breaking the bank. Made from type III hardcoat anodized...
www.pantheonarms.com www.pantheonarms.com
Click to expand...
"Reinfection" may be down to viral RNA still present like you've said, I would not expect reinfection to happen so fast for a disease, I've heard about viral RNA presence long after infection so I'd assume this is the case.

I also agree that TCM is a load of shit, I've seen papers stating some TCM works as a treatment against CoV-2 and I highly doubt those papers are actually true.

The vast number of clinical symptoms is likely due to the infiltration of multiple different cell types, the virus itself isn't doing shit other than getting cells flagged as infected by the immune system.
This goes in line with the large degree of inflammation and immune cell infiltration in organs seen in patients.

Interesting to see the conflicting reports regarding ARBs, it'd further support the need for some sort of antiviral in any treatment involving ARBs, but that should be a given.

It's not the virus, it's the virus making the immune system flip its shit everywhere in the body.

The more I read, the more I suspect means of preventing cell entry would be the most crucial aspect of treatment as it'd prevent it from entering cells and causing the immune system to essentially do its job for it. You'd then need something to keep the immune system in check as patients taken to the clinic will likely have this happening, and then treatments for other issues such as excess angiotensin 2.

By this end, I'd assume in patients with strong immune systems, it just simply gets cleared before it starts infiltrating all over the place, but in those with worse immune systems it is given the chance to do so, leading to what you see in the clinic.

To summarize:
Strong immune system sees virus -> clears it up before it can do much -> Nothing really happens
Not so good immune system can't clear it fast enough -> CoV-2 infiltrates various cell types, can't actually do much within them and instead gets the cells flagged as infected -> Immune system shits a brick, the noted cytokine storms and various clinical symptoms occur

Edit:
This is probably fairly rushed as a post as I'm currently trying to get some work done.
The virus to me doesn't seem like a cloud of death, it's using its easy access to cells via the furin cleavage site in the S protein to get into cells and it's causing the immune system to freak out in some patients. We should aim for keeping viral load down and also making sure the immune system isn't going nuts in patients.

I've also found a paper demonstrating the effectiveness of a synthetic consensus anti-spike protein DNA vaccine for MERS

https://www.ncbi.nlm.nih.gov/pubmed/26290414

This is honestly pretty great for me to find, MERS is a fellow coronavirus, so perhaps we can look at a similar vaccine for CoV-2, which I'm sure is being done as of writing.
 
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Drain Todger said:
Here, for a laugh, watch my fat ass make a fool of myself and brass myself in the face with my .50 AE Deagle, leaving a perfect Hornady headstamp mark stamped right on my forehead.

Click to expand...
That description :story:
Screen Shot 2020-04-14 at 20.51.27.png

Archive:
 
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evrae said:
"Reinfection" may be down to viral RNA still present like you've said, I would not expect reinfection to happen so fast for a disease, I've heard about viral RNA presence long after infection so I'd assume this is the case.

I also agree that TCM is a load of shit, I've seen papers stating some TCM works as a treatment against CoV-2 and I highly doubt those papers are actually true.

The vast number of clinical symptoms is likely due to the infiltration of multiple different cell types, the virus itself isn't doing shit other than getting cells flagged as infected by the immune system.
This goes in line with the large degree of inflammation and immune cell infiltration in organs seen in patients.
Click to expand...

That's very true, but there are actually a few different mechanisms at work, here. One of the primary mechanisms of injury is the huge host response that it causes, of course. This is a property it shares with SARS, which also did the lion's share of its damage by cytokine release syndrome.

However, the virus uses up ACE2 receptors and dysregulates the RAAS, too. It could be causing focal hypertension, in addition to the hypokalemia that it's causing. The excess of Angiotensin II is causing renal wasting of potassium. In other words, it leads to an electrolyte imbalance. A successful treatment regimen of COVID-19 patients may involve potassium replacement, as a consequence.


Furthermore, a recently concluded study showed that severe and critically ill patients with COVID-19 had a higher prevalence of hypokalemia that resulted from renal potassium wasting. This can be explained by downregulation of ACE2 following viral intrusion resulting in decreased degradation of angiotensin-II, increased aldosterone secretion and subsequent increased urinary potassium loss. Infact early normalization of serum potassium has been proposed to be a predictor of good prognosis in COVID-19 [16]. Thus, ACE2 overexpression, while facilitating entry of SARS-CoV-2, is unable to protect against lung injury as the enzyme gets degraded by the virus (see Fig. 1) .
Click to expand...

The other thing it's doing is promoting bacterial co-infections by its attack on the immune system (the lymphopenia might have something to do with it). This could lead to bacteremia and sepsis. In many cases, they've been giving patients prophylactic antibiotic treatment to try and forestall the development of secondary infections.

Various antibiotics are being tried. There's the much-vaunted azithromycin, you know, the Z-Pak, but there are also other ones that they're testing out, I hear.

evrae said:
Interesting to see the conflicting reports regarding ARBs, it'd further support the need for some sort of antiviral in any treatment involving ARBs, but that should be a given.

It's not the virus, it's the virus making the immune system flip its shit everywhere in the body.

The more I read, the more I suspect means of preventing cell entry would be the most crucial aspect of treatment as it'd prevent it from entering cells and causing the immune system to essentially do its job for it. You'd then need something to keep the immune system in check as patients taken to the clinic will likely have this happening, and then treatments for other issues such as excess angiotensin 2.

By this end, I'd assume in patients with strong immune systems, it just simply gets cleared before it starts infiltrating all over the place, but in those with worse immune systems it is given the chance to do so, leading to what you see in the clinic.

To summarize:
Strong immune system sees virus -> clears it up before it can do much -> Nothing really happens
Not so good immune system can't clear it fast enough -> CoV-2 infiltrates various cell types, can't actually do much within them and instead gets the cells flagged as infected -> Immune system shits a brick, the noted cytokine storms and various clinical symptoms occur
Click to expand...

Yes, exactly!

I saw an article over a month ago where they were talking about blocking the priming of SARS-CoV-2's spike using Camostat, a protease inhibitor.


The recent emergence of the novel, pathogenic SARS-coronavirus 2 (SARS-CoV-2) in China and its rapid national and international spread pose a global health emergency. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets. Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S-driven entry. Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention.
Click to expand...

I think they're planning on trials with Camostat pretty soon. I don't see any data on efficacy yet:

clinicaltrials.gov

Combination Therapy With Camostat Mesilate + Hydroxychloroquine for COVID-19 - Full Text View - ClinicalTrials.gov

Combination Therapy With Camostat Mesilate + Hydroxychloroquine for COVID-19 - Full Text View.
clinicaltrials.gov clinicaltrials.gov

Now, to the part that actually had me creeped out about all this. The apparent neurotropism of the virus.

In this old mouse study with transgenic hACE2 mice, they challenged the mice intranasally with the related SARS-CoV. The virus actually entered and infected the olfactory bulb, and it infected the cardiorespiratory center of the medulla and depressed the breathing of the lab mice, leading to aspiration pneumonia (the mice "forgot" how to breathe). It's also worth mentioning that anosmia is a frequent symptom of this virus. Is it infecting people's olfactory nerves?


Then, I saw this. There was another study where they were claiming that people were having neurological symptoms, like headache and depressed breathing, and they were claiming that the "mechanoreceptor and chemoreceptor nerves of the lungs" may allow the virus to infect the brain stem through a "synapse-connected route":


When I heard this, my thought was, you know, it sounds like they're saying this thing can enter the parasympathetic nerves of the lungs, climb into the vagus nerve, and then enter the medulla.

I thought, y'know, that's some real scary shit.

Then, all these other articles seemingly confirming neurotropism started showing up:

Neurological Manifestations of Hospitalized Patients with COVID-19 in Wuhan, China: a retrospective case series study

OBJECTIVE: To study the neurological manifestations of patients with coronavirus disease 2019 (COVID-19). DESIGN: Retrospective case series SETTING: Three designated COVID-19 care hospitals of the Union Hospital of Huazhong University of Science and Technology in Wuhan, China. PARTICIPANTS: Two...
www.medrxiv.org www.medrxiv.org




By that point, I'd seen numerous leaked videos on social media of people collapsing and seizing on the ground with abnormal posturing, their legs extended out straight and rigid like drowning victims and their arms crossed over their chests or down at their sides (decerebrate/decorticate posturing), or even the fencing response (one arm sticking straight out from the chest), and I was like... "holy shit, this is neurological".




This was why I panicked and spilled my spaghetti across half the internet.

There's little-to-no official acknowledgement of the neurotropism of this virus, or these collapses and seizures. We don't even know how often this happens, or if these videos were taken out of context, or what.

It's all up in the air.

So, @evrae I ask you, was I right to be concerned?

Was I on the right track, or not?
 
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Drain Todger said:
Sperging
Click to expand...
Dude, you really need to tone it down. Getting into internet fights on this autistic site isn’t worth it. This is the equivalent of screaming into a void.

If you really need to make yourself known, learn to use more brevity. This isn’t a college class, so this many citations in one post is ridiculous. Learn to use fewer words. It’s a good thing there is a word limit for posts on the Farms, because if there wasn’t, we would be having even longer posts from you. Unless you’re writing the OP for your lolcow thread (which you practically did in this thread), nobody needs to read posts that long.
 
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Ped Xing said:
Also, post more about yourself and less about the coof. We all already know about the latter.

"No comment" on a silly question makes my antennae vibrate. Enhance.
Click to expand...

I'm a lonely, ugly, pimply, spergy, masochistic, gorilla-shaped sack of lard who writes My Little Pony fanfics. Not a winning hand in the game of love, by any stretch of the imagination.
 
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Drain Todger said:
I'm a lonely, ugly, pimply, spergy, masochistic, gorilla-shaped sack of lard who writes My Little Pony fanfics. Not a winning hand in the game of love, by any stretch of the imagination.
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There is a distinct lack of nudes there.
I guess the hugbox in that one forum I can't be bothered to remember the name of doesn't like you enough. One cocksucker is never enough.
 
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Ugly can't be fixed, but humor aside it's not like you're some sort of mutant freak.

But yeah, you need to fix your personality and get in shape. That will allow you to fix the "lonely" part. That and moving out of Daddy's Duplex seriously wtf.

Tellyawhat. "Masochistic" is not a problem. Register a Train Dodger Fetlife, and we will observe and advise. I know several kiwis are already trying to matchmake you.
 
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