How does coronavirus kill? Clinicians trace a ferocious rampage through the body | Hacker News Reader

How does coronavirus kill? Clinicians trace a ferocious rampage through the body

sciencemag.org

110 pointsdoener47 comments

I'm home with Covid-19 right now. I'm an intensivist and probably got infected at work. That's also why I had access to PCR testing to confirm the diagnosis after only two days of symptoms.

I'm 36, in good shape, was lucky, and one week in I'm feeling stronger every day.

It wasquite unlike any other "flu" I've had.

What was the symptom progression like? Did you feel better and then worse again at any point before feeling better again?

First a cough that got a bit worse over a night shift. Then fever. Lots of clear mucus from the lungs. I never had any problem breathing but got a bit worried with the amount of mucus and coughing.

Like many have reported my sense of smell is completely gone. That happened after about two days.

About 5-6 days in now I still feel tired and probably have a light fever although I haven't bothered to measure. I'd say I've been getting steadily better but slowly.

Is the lose of smell due to mucus build up? Or something more scary like directly affecting the brain's ability to process smell based input? (Or more likely somewhere in the middle?)

It's not because of mucus. Unlike a normal flu I've not had a runny nose, at all.

Will be interesting to learn more about this once it is all over. Get well soon.

Thanks!

A potential mechanism is discussed in the article:

> Last month, Sherry Chou, a neurologist at the University of Pittsburgh Medical Center, began to organize a worldwide consortium that now includes 50 centers to draw neurological data from care patients already receive. The early goals are simple: Identify the prevalence of neurologic complications in hospitalized patients and document how they fare. Longer term, Chou and her colleagues hope to gather scans, lab tests, and other data to better understand the virus’ impact on the nervous system, including the brain.

> Chou speculates about a possible invasion route: through the nose, then upward and through the olfactory bulb—explaining reports of a loss of smell—which connects to the brain. “It’s a nice sounding theory,” she says. “We really have to go and prove that.”

I heard the median time for hospitalization is 10 days after first symptoms, so continue resting and taking care of yourself.

I am also a healthy man in my mid thirties, and like you, got infected and quickly recovered. That a was a month ago.

It would be good to know if the organ damage detailed in the article also affects those that recover without significant symptoms.

I fear it does, because I have lost and not regained my sense of smell.

I'm not too worried about that (yet). I think you have a good chance to get it back but it will probably take a while.

Glad you are recovering so quickly !

Quick question: is 'viral load' a thing ? I have read in several places that repeated contact with infected people is an important factor to determine disease severity.

I'm not an expert in virology but I think there are some theories that a larger exposure could potentially lead to more serious disease.

I think I had it as well. A good month and a half to two months ago. But there was no testing where I live, and antibody tests doesn't exist here yet.

But as you say, a weird "flu".

My doctor recommended minimal doses of Cyproheptadine+DHEA+Progesterone to help heal my ex-smoker lung. I'm guessing the same could be useful for recovered COVID-19 patients and am not seeing it mentioned much, so I thought I'd chime in.

https://www.eurekalert.org/pub_releases/2016-09/p-pph090816....

I read somewhere, that COVID-19 attacks alveoli first, in contrast with other viruses who start with attacking bronchi. It leads to problems with bloog oxygenation, but human body doesn't control for oxygen levels, monitoring instead levels of CO2. So it leads to hypoxia which goes undetected for a some time. Damage to alveoli also goes undetected, because alveoli lack pain receptors.

I'm not a medic, I don't know is it plausible explanation or not (I'm even not sure whether I succeeded to use correctly all the anatomical words like "bronhi" or "alveoli") but I'd like someone knowledgeable to comment on this. I wander if it was true, could hypoxia explain other symptoms, like heart damage.

This theory doesn't seem plausible, the very place where the body releases CO2 is the same for O2.

The comment about "not controlling for O2" is referring to the fact that the human body can't directly detect blood oxygen levels, and only infers them from blood CO2 levels. So if something's going wrong with the oxygen absorption process but the CO2 exhalation process is still fine, that would explain why patients have dangerously low blood oxygen but aren't panting or otherwise showing respiratory distress.

(Incidentally this is also why it's really dangerous to hyperventilate before free diving, because you can put your O2 / CO2 ratio out of whack which can cause you to black out without warning while under water.)

> the human body can't directly detect blood oxygen levels, and only infers them from blood CO2 levels

This is not quite accurate. The body monitors blood chemistry centrally (in the brain and spinal cord) and peripherally (in the blood vessels).

Central chemoreceptors only monitor pH of the cerebrospinal fluid, which indirectly tracks blood CO2, but don't monitor O2.

Peripheral chemoreceptors monitor O2, CO2, and pH.

https://courses.lumenlearning.com/boundless-ap/chapter/respi...

But there there was low levels of O2, wouldn't it mean low levels of CO2? Body doesn't have enough O2 to produce much of CO2, seems plausible for me.

CO (carbon monoxide) poisoning happens the way it does for this reason: You don't feel lack of oxygen - you feel abundance of (uncleared) CO2. If you have too much CO, you lack oxygen but don't have too much CO2, you just feel sleepy/drowsy but suffocate and die unless you do something.

Whether the rest of OPs theory makes sense, I don't know - but this part is indeed factual AFAIK.

The virus appears to impair hematic function in the lungs. The oxygen builds up, and it is quite caustic. It creates what are called ground glass bodies. Since the oxygen is trapped in the lungs and does not move the blood very efficiently, you get hypoxia.

A few weeks ago they were investigating symptoms similar to HAPE - High Altitude Pulmonary Edima.

Basically, you get blood clots and those go into the heart to the lungs and block the blood vessels (killing parts of the lungs) and presumably other parts of the body. You also get the cyto storm.

So it's not surprising that it's causing damage everywhere. I wouldn't be surprised if asymptomatic people have some damage, but not enough to cause noticable symptoms.

The article has a section that talks about how the virus affects the brain and that the low oxygen level is because the virus may somehow suppress the brain stem reflex that causes gasping when oxygen levels are low.

> human body doesn't control for oxygen levels, monitoring instead levels of CO2. So it leads to hypoxia which goes undetected for a some time.

I don't think that's quite correct. Hypercapnia (excess CO2) triggers a reflex to inhale, that's what you feel when you hold your breath for a long time. That reflex doesn't trigger when you're inhaling CO, for instance.

But the body does have sensors to detect oxygen levels in the carotid body (and maybe the aortic body?). These do impact breathing as well, but they do so via the parasympathetic nervous system so you're not as aware of it. IIRC the way this works is poorly understood, and its dysfunction been thought to play a role in sleep apnea.

That would possibly explain why some people have trouble with oxygen deprivation in high altitudes while others inexplicably do not. I wonder if people who see a lot of benefit from breathing techniques like Pranayama and Wim Hoff have issues with that mechanism.

Anything that overruns the body will kill in diverse ways.

Cancer does the same thing. This isn't something new and terrifying...

A supercomputer probably couldn't model the exact way a terminal cancer patient will die.

Partially agree with this. It is not uncommon for a virus to sneak into the brain or other organs, but SARS COV2 is a little different in that it specifically attacks receptors found in all those areas. It isn't just a bi-product of the virus overwhelming your immune system and being so prevalent it gets into everything.

I do wish these articles would talk more about what the virus is doing (less scary) than what it can do (article can be written to be as terrifying as the author wants). If .0000001 of cases have their hearts attacked it isn't as fear mongery as saying "look it can attack your heart!"

There's just not much of an article to write about what the virus generally does. They lay out the typical course over two paragraphs near the beginning of the article: it infects the lungs, and gives patients a progressively harder time breathing, until either their immune system fights it back or their breathing is too impaired.

Cancer is terrifying.

"the virus acts like no pathogen humanity has ever seen"

Really? Is that not hyperbole?

The devs really need to nerf it in the next patch.

So we have: Direct massive attacks to 1) Lungs (plus capillaries) with or without sensation of asphyxia and 2) Kidneys (renal failure) as the two main battlefields.

Also to 3) brain/olfactive centers in nose and 4) could reproduce also in gut (maybe with a low risk of transmission by faeces).

And we can be caught also in the friendly fire of citokinine storm, but liver damage is probably unrelated with coronavirus

Very interesting article.

... and heart damage, I forgot it.

Could be blood clots going literally everywhere in the body.

I know somebody with a serious blood clotting disorder. I can’t find research about whether they are higher risk or not. Does anybody know of a study that looked at this?

I think there is a previous discussion from a couple of weeks ago

Truly terrifying

With an average diameter of 0.1 micrometers it is extremely stable for 2 weeks at 4°C and survives for 5 minutes at 70°C and active while airborne for up to 3 hours

Yes, it's entire possible that the "cytokine storm" hypothesis turns out to be wrong. Here's my inexpert summary of what some researchers believe: A buildup of superoxide radicals leads to a buildup of other "reactive oxygen species," all of which cause acute oxidative stress—notably in the endothelia.

So COVID-19 attacks the endothelial structures throughout the body. Notably the interface between lungs and blood vessels, but also the heart, other vital organs, capillaries, etc. Hence clotting and "sticky blood" is a huge problem.

Unsurprisingly, bad diet messes up one of the pathways the body uses to cleans up superoxide radicals—chronic high sugar and lack of trace elements (zinc, copper, magnesium). And now it seems C19 messes up another pathway, thanks to it interfering with ACE2 receptors. This could be why we're seeing high mortality in people with diabetes, pre-diabetes, and all the other conditions related to poor blood-sugar regulation—obesity, coronary artery disease, dementia, etc.

A good summary at: https://www.youtube.com/watch?v=Aj2vB_VITXQ

Vitamin D appears to be playing a large role as well. I wondered why France wasn't hit harder and all I could come up with was wine (antioxidant) and cheese (vitamin D from dairy). India is another country that follows this pattern tumeric (antioxidant) and dairy.

There is (virtually?) no vitamin D in cheese. Milk is fortified with vitamin D in some places, maybe that's what you're referring to?

France has been hit extremely hard though.

Are they still not including deaths in retirement homes as part of the fatality count or did they backtrack on that?

They are Included in the daily reports since beginning of April IIRC. The total number of fatalities also includes losses in retirement houses for March.

India has an extremely stringent lockdown.

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