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MarineLife42 t1_iuxe9d2 wrote

Viruses don‘t necessarily cause cells to die, or go into lysis. Bacteriophages do that, but as the name suggests, they affect bacterial cells, not Eukaryotes.

Ebola is a virus that causes cells to die and burst, which makes it so lethal.

On the whole, though, a virus has no interest in killing its host because the dead can‘t spread the virus. So most viruses that affect humans, including Covid, use different strategies. They infect some cells but not all, and the infected cells stay alive - although their function is now to produce new viral particles while their normal, healthy function is suppressed.

For the individual person, it then depends on how many cells got infected and which type they are. We know that SARS-CoV19 likes to enter the cell through the ACE surface protein. Different people have different amounts of these surface proteins on their cells, and in different tissues. E.g. if you have lots of ACE surface protein in your nose and lungs, then those tissues will be mostly affected. If they are absent there but you have some in your bone tissue, expect that area to be affected by the virus.

Then there are those who have very little ACE surface protein in the first place, so they don‘t experience many symptoms. This doesn‘t stop their immune system from attacking the intruder and making antibodies, however.

In all that is only part of the story, though. The research is still very much ongoing and there is not yet a conclusive answer for why some people die from Covid and others don‘t even notice they have it. A few predisposing factors have been identified, but Covid is not only a new virus, it is also constantly changing so that basically both the ball and the goalposts move all the time.


Chewie83 OP t1_iuxs7ml wrote

Great info, thanks! I thought (incorrectly) that infected cells were almost always killed, either by the virus or by the immune system itself —like how our bodies attempt to kill cells that are becoming cancerous.

I’ll have to read more about how infected cells can be told by the immune system to stop printing more viral particles without being killed in the process.


DiscordAccordion t1_iuzhf11 wrote

Quick correction: bacteriophages do not all go lytic. A great number are temperate phage, which integrate into the genome of the host cell and are replicated as the host divides. When the host is stressed or damaged, the phage will excise itself and go lytic.


turtlechef t1_iuzmq30 wrote

Do you have any sources on what you wrote eabout people having different #s of ACE proteins? Just out of curiosity. I didn't know that people had dramatically different numbers of ACE proteins


MarineLife42 t1_iuzxci0 wrote

I can‘t point you to specific papers at the moment because I am at home where my access is limited. Here‘s a link to a number of papers going in that direction. As you can see, they not only explore the location of the ACE2 protein but also the small variations between the proteins that people exhibit.


Nyrin t1_iuxcnr9 wrote

Asymptomatic infections can create damage and it's a very real problem.

For example, it's a concern that there are observed, enduring differences/abnormalities in the lungs of even asymptomatic COVID-19 convalescents that could greatly complicate future treatments, e.g. here in radiation therapy for certain cancers:

Along with more publicized "long COVID" sequelae, these kinds of things are why the myopic focus on fatality rates throughout the pandemic has been so stupid; for every already-at-risk person killed by a primary infection, there are hundreds, thousands, or even more who are going to experience some degree of complexity in the onset, management, and treatment of future problems, many of those patients having noted little or no acute symptomology during primary infection.