Does anyone have a good article/video/infographic that details, step-by-step, the progression of an omicron infection through your body?
Not just what happens within the cell, but the path of a typical infection through your body, the particular cells it infects to do so, and the various ways it damages your tissues, organs and immune system.
I found this one recently about what happens in the cell itself, for your enjoyment: https://www.youtube.com/watch?v=XlOi2hVGtg0
It pretty much blindly does this to every cell. It hits cells with more ACE2 receptors more often.
It works its way mechanically through the nose, lungs, and then into the bloodstream, and from there to whereever it can get (brain, etc.)
It also produces special chemicals to screw up the immune system, I don't fully understand those but they're documented. That could use a video.
@neroden That's what I'm hoping to do, I just bought new animation software.
I know the basics, but I'm not certain of the details of the progression. I want to detail it in a way that describes which cells in the nasal cavities are infected, then how it progresses to T Cells using them to transport around to other organs, what it does to those T Cells, which organs it tends to hit first, and also how it can progress up the olfactory nerve to invade certain parts of the brain.
1/2
It definitely seems to be quite random which organs it hits hardest. Every cell in the body has ACE2 receptors, so I think it's luck which determines whether it hammers your brain or your kidneys.
It seems to go mucus membranes->blood->rest of body, I don't think one can be more specific than that
@neroden @toba
But for a "typical" mild case (I use that term lightly) we have an approximate timeline of the progress.
I want to show how it reaches the different organs (there are a few mechanisms, including use of the T Cells for transport*) and which tissues in those organs they are infecting, and perhaps list what kind of comorbidities for other diseases and medical issues that damage can cause.
* Edited to remove: fairly early on, which doesn't get discussed in mainstream content much
Visualization of virus particles in plasma indicates that SARS-CoV-2 RNAemia is due, at least in part, to viremia. The levels of SARS-CoV-2 RNAemia correlate strongly with disease severity, patient outcome, and specific inflammatory biomarkers but not with neutralizing antibody titers.
Hmmm... I was under the impression that the T Cell infection was a regular mechanism, vs a rarity, but it appears to be more associated with severe disease.
"Infected T lymphocytes not only lost the ability to control viral infection but may also carry viruses to other parts of the body through blood circulation."
https://www.nature.com/articles/s41392-022-00919-x
SARS-CoV-2 induced marked lymphopenia in severe patients with COVID-19. However, whether lymphocytes are targets of viral infection is yet to be determined, although SARS-CoV-2 RNA or antigen has been identified in T cells from patients. Here, we confirmed that SARS-CoV-2 viral antigen could be detected in patient peripheral blood cells (PBCs) or postmortem lung T cells, and the infectious virus could also be detected from viral antigen-positive PBCs. We next prove that SARS-CoV-2 infects T lymphocytes, preferably activated CD4 + T cells in vitro. Upon infection, viral RNA, subgenomic RNA, viral protein or viral particle can be detected in the T cells. Furthermore, we show that the infection is spike-ACE2/TMPRSS2-independent through using ACE2 knockdown or receptor blocking experiments. Next, we demonstrate that viral antigen-positive T cells from patient undergone pronounced apoptosis. In vitro infection of T cells induced cell death that is likely in mitochondria ROS-HIF-1a-dependent pathways. Finally, we demonstrated that LFA-1, the protein exclusively expresses in multiple leukocytes, is more likely the entry molecule that mediated SARS-CoV-2 infection in T cells, compared to a list of other known receptors. Collectively, this work confirmed a SARS-CoV-2 infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID-19 patients.
Brittany
Nathanael Nerode
Eric Stein �