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Just_Observational t1_iy4osc3 wrote

Quick tip, for questions where you're referencing specific functionality of a virus google scholar will be your best bet at finding a free available article which can answer your question.

The answer if it's a college quiz question is probably going to be found in the last paragraphs.

How specific are you looking for? That would help a lot with this as you seem to be familiar with some of the terminology but not the specifics of the functionality? College student? If this is for an assignment ask your professor/teacher directly, there is debate still within the scientific community about a fair bit of the functionality of Covid-19 and they may want a specific answer and can point you to their source of information.

That being said, most viruses will penetrate a number of ways into the system to cause a systematic infection. Autoimmune viruses tend to favor lymphatic tissues or pulmonary infection where pox viruses will infect through the epithelial skin layer, after absorption by host via their preferred pathway they tend to migrate to the point where host cells are most prevalent as that's where they proliferate so mutation favors those infection pathways. For Covid-19 those preferred host cells are readily available as their favored cells tend to be epithelial mucosal cells.

If however Covid-19 resides in the host long enough, proliferates quickly enough, or any other number of things can happen you can get Covid-19 in the blood stream at a viral load that is capable of causing organ infections as most organs contain the ACE2 receptor which is the primary way that Covid-19 will undergo attachment. There is another receptor they use but with sufficient load you can get liver, brain, and heart infection as well.

The specifics of how each point of entry through the epithelial layer is different for each of the epithelial systems. Covid-19 causes clotting in many narrow arteries which is one method for viral load to reach a critical point of infection that it can penetrate to the circulatory system.

Since you mentioned Type II Pneumocytes I will focus on those. They are found on alveolar surface and are a typical infection cell and pathway into the system. Specifically I'm guessing with reference to this cell type your question is referring to Covid-19 Pulmonary infections and symptomatic ARDS which are generally triggered by infection and lycing of type II Pneumocytes in the alveoli. That is one correct answer to how a typical Covid-19 infection can turn systematic.

If anyone sees any issues in the information I've presented please feel free to post a correction, I did not get a chance to proof this as I am getting busy with my work now. I tried to keep this to an undergrad level with the OP sounding like an undergrad or curious high schooler asking about a quiz or homework question.

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cl174 t1_iy7c99h wrote

I think the better answer would be that we (probably) don't know the mechanism, and while all of these are probably decent guesses/plausible potential mechanisms, we don't really know how because it's a relatively difficult question to study.

Additionally, some of the few viruses that I have seen it relatively well characterized are surprisingly complex mechanisms, like HIV's route from various mucosal surfaces into the body and then onto T-cells. So even though everything you mentioned here seems plausible, I also wouldn't be shocked if the reality is completely different.

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Just_Observational t1_iy7o3dk wrote

We have a collection of peer reviewed research on some mechanisms for entry due to other viruses allowing us to infer from other 'similar' viruses and confirm the portal of entry by studying tissues of affected individuals.

What's called the chain of infection within virology tends to follow similar modes of entry for similar viruses. Generally the main differences between species and sometimes individuum are that they targeting different receptors of the same cells. The studies showed that under study the physiological reaction to infection indicated that the portals of entry that have been hypothesized are significant in their likelyhood as portal of entry.

Do you have peer reviewed research for me to read that states differently? I most likely have access to it if you do have one.

This subject has been researched heavily since the onset of the pandemic and there's a lot of peer reviewed research. Some fraudulent articles as well, so make sure they're properly reviewed.

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Megodont t1_iy4g8sg wrote

As far as I unterstood it (not an expert) the main entry point are epithel cells in the nasal cavity and upper respiritory track. These areas are full of blood vessel. I would guess, the infection of the lung comes from the blood vessel into the alveoles.

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