I've been quiet about this issue for a long time but some things are worth writing about. To me, anyway. I work for someone who absolutely cannot afford to get sick, particularly with any respiratory illness.

The article posted here is quite long and goes deep into the weeds of mutations and subsequent structural changes to viral protein binding regions. This information is providing some of the data needed for understanding what goes on in those unlucky 10% or more that wind up with long COVID. As somewhat of a summary, I'll say this before the article below.

Depending on the mutations in whatever variant a person contracts, they can wind up with a COVID-19 infection capable of invading a subset of lymphocytes. It depends on what mutations are in the viral N-protein of their invading COVID-19 as opposed to the different characteristics of the spike protein. This situation does not go away and it weakens the immune system. While it isn't the same as what HIV does, this effect is properly classified as an acquired immune deficiency syndrome.

The spike protein we've all heard about binds ACE2 (angiotensin converting enzyme 2) in the process of invading various cells in our bodies. However, lymphocytes don't have a lot of ACE2 so the spike protein isn't very important for COVID-19's ability to invade them. What is important is CD147, a complex protein that sits in the plasma membrane. The virus' N protein binds it and some mutations make it much easier for COVID-19 to bind, invade the cells and continue to make more of itself. Among many things it does, binding CD147 is also implicated in the blood vessel damage and blood clotting some people get with COVID.

Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes

https://www.sciencedirect.com/science/article/pii/S2319417023000872

PeterWick said:

I've been quiet about this issue for a long time but some things are worth writing about. To me, anyway. I work for someone who absolutely cannot afford to get sick, particularly with any respiratory illness.

The article posted here is quite long and goes deep into the weeds of mutations and subsequent structural changes to viral protein binding regions. This information is providing some of the data needed for understanding what goes on in those unlucky 10% or more that wind up with long COVID. As somewhat of a summary, I'll say this before the article below.

Depending on the mutations in whatever variant a person contracts, they can wind up with a COVID-19 infection capable of invading a subset of lymphocytes. It depends on what mutations are in the viral N-protein of their invading COVID-19 as opposed to the different characteristics of the spike protein. This situation does not go away and it weakens the immune system. While it isn't the same as what HIV does, this effect is properly classified as an acquired immune deficiency syndrome.

The spike protein we've all heard about binds ACE2 (angiotensin converting enzyme 2) in the process of invading various cells in our bodies. However, lymphocytes don't have a lot of ACE2 so the spike protein isn't very important for COVID-19's ability to invade them. What is important is CD147, a complex protein that sits in the plasma membrane. The virus' N protein binds it and some mutations make it much easier for COVID-19 to bind, invade the cells and continue to make more of itself. Among many things it does, binding CD147 is also implicated in the blood vessel damage and blood clotting some people get with COVID.

Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes

https://www.sciencedirect.com/science/article/pii/S2319417023000872

Wow! That's fascinating. Thanks for sharing. It's a strange virus, but so is HIV...

ETA: Would have been better if there weren't a major typo in the main conclusion: "Acquire Immune Deficiency Syndrome."