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.

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.

Rule of thumb, if a food place is open in California and is Mexican, even a chain, it's going to be damn good food. Except Del Taco.