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COVID-19 is not a normal respiratory infection. It seems to prevent your RBCs from holding onto O2 and CO2 mimicking high altitude sickness. The disease acts like HAPE (high altitude pulmonary edema). The damage and inflammation is coming from the blood's inability to properly perform gas exchange in the lungs. Other damage could actually be coming from ventilators with pressure set too high (lungs of patients are mechanically normal, atypical for ARDS). Patient oxygen stats are also weird, they're hypoxic, but not necessarily short of breath.

Thank you for posting this - some of the other comments didn't quite capture it. See the twitter of Cameron Kyle-Sidell who is working at Maimonides Hospital in Brooklyn for additional info. https://twitter.com/cameronks/status/1246765252307533825 https://www.medscape.com/viewarticle/928156

> Chloroquine prevents the virus from affecting hemoglobin

This virus attacks the cells that live in the throat and lungs. The "spike" as far as I'm aware does not attach to haemoglobin.

> damage is already done and the hemoglobin is already compromised.

Its the lungs that are damaged, not the blood. The reason why people die is because they drown in thier own fluids, as the cells walls of the lungs are broken down by the patient's immune system.

If Chloroquine was effective, it would stop the virus reproducing. This would lead to a detectable change in viral load.

Sure, it could already be to late by then, the damage is done. But, the viral load would have a measurable change. These studies don't really show anything conclusive.

This means that its unlikley to work as a prophylactic as its not actually stopping the virus from attaching or reproducing.

> Azithromycin

Thats there to stop any opportunistic bacteria from causing more damage. Typically when someone is admitted to ICU for covid they have a lower than expected white cell count.

> Antivirals are much more promising

yes because they actually disrupt the virus replicating. Chloroquine doesn't appear to do that. This is the problem with making drugs. Something that works in the petridish doesn't always work in the body. This is why Gilead's new wonder drug wasn't in production, because it was designed to target ebola, but didn't really work.

> as the cells walls of the lungs are broken down by the patient's immune system

If there is actually a real statistical anomaly that Lupus and other immune comprised people are less susceptible to certain parts of the virus, perhaps it's not the medication they take at all. It could simply be that someone who is immune compromised would not have as strong as a reaction as a healthy person and then may actually survive as a result. Less fluid, etc. Also, I am in no way qualified medically, it's just a quarantine showerthought.

I have heard of two patients in london who were immuno compromised and recovered quicker than a "normal" person.

The real damage occurs when the immune system ramps up to attack the virus, but ends up attacking the cells they are living in as well. Now, most of the time this is fine an normal, but it can also trigger https://en.wikipedia.org/wiki/Cytokine_release_syndrome which is a nasty feedback loop.

There are experiments to give immuno-suppressants at key times to try and limit the damage. But its tricky and dangerous.

COVID-19 is not a normal respiratory infection. It seems to prevent your RBCs from holding onto O2 and CO2 mimicking high altitude sickness. The disease acts like HAPE (high altitude pulmonary edema). The damage and inflammation is coming from the blood's inability to properly perform gas exchange in the lungs. Other damage could actually be coming from ventilators with pressure set too high (lungs of patients are mechanically normal, atypical for ARDS). Patient oxygen stats are also weird, they're hypoxic, but not necessarily short of breath. https://vimeo.com/402537849 https://twitter.com/EricLeeMD/status/1245054768185303041?s=1.... https://twitter.com/cameronks/status/1243582723945566208?s=1.... https://www.cureus.com/articles/29004-acetazolamide-nifedipi....

> If you want to detour into tinfoil hat territory, you could posit that these studies on severe patients were designed knowing it would show low or no efficacy, because it’s too late to protect the patient’s hemoglobin.

I would think it is still useful because from what I've read, this protocol is often used for severe cases at the moment, so it's useful to know if it has no impact.

Very true. It does make sense to look at those in the most dire need first. That did not occur to me.

Isn't that paper highly theoretical at this point since it's based on computer simulations? Are there any studies on actual humans confirming the virus's effect on hemoglobin?

These papers are older and in regards to malaria, but the mechanism in regards to hemozoin is theoretically the same:

https://www.nature.com/articles/s41598-019-51604-z

https://www.sciencedirect.com/science/article/abs/pii/S00207...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4928194/

https://www.pnas.org/content/114/29/7483

If that hypothesis correct then we should be able to test it with blood transfusions, or possibly hyperbaric oxygen therapy (HBOT). HBOT can be used to treat patients with severe carbon monoxide poisoning. Even though their hemoglobin is unavailable, enough oxygen dissolves into the blood to prevent ischemia.

That only works if the lungs are viable. In this case they are so damaged they just fill up with fluid. Thats the issue.

effectively the patients drown. Its not like CO poisoning at all.

"COVID-19 attacks hemoglobin and that is how it damages the lungs."

COVID-19 is not the virus, it is a disease cause by SARS-CoV-2.

And no, SARS2 does not "attack hemoglobin". The lungs are filled with fluid from an overly zealous cytokine response and the bacterial infections that follow.

See this comment, with sources: https://news.ycombinator.com/item?id=22798543

Azithromycin helps with pneumonia which is a common progression of covid.

There's literally no proof of this. It's based on a paper that's purely untested conjecture and hypothesis right now.