![How COVID actively suppresses and evades your immune system [Part 2]
Part 2 looks at how mild and m...](https://pbs.twimg.com/media/Fl8zfaRXEAAacYA.jpg)
An unrolled one-page web view for both parts of this long thread that may be easier to read or share can be found here ( ). 2/
If you haven't read part 1 yet on how the virus hides from T-cells and NK immune cells you can find it here: 3/
Monocytes are a type of white blood cell in the immune system which can defend against infection by cleaning up damaged cells and can differentiate (transform) into two other types of cells: Dendritic and Macrophage ( my.clevelandclinic.org ). 4/
Dendritic cells call on other immune cells for help and can present viral proteins (antigens) on their cell surface to T-cells for them to learn how to identify and destroy. They can also act as messengers between the innate and adaptive immune systems. 5/
Macrophages surround an invading pathogen, ingest, and kill it with toxic enzymes within the cell. They also help remove dead cells from your tissues and bloodstream. 6/
You can learn more watching this @Kurz_Gesagt "How your immune system actually works video" ( youtube.com ) and @VirusesImmunity "Immunology 101 for non-immunologists video" ( youtube.com ) and. 7/
A study looked at patients with mild & moderate COVID and found monocytes from COVID patients had altered cell surface receptors & a dysfunctional metabolic profile that makes them identifiably different than healthy monocytes ( nature.com ). H/T: @fitterhappierAJ 8/
Researchers could even clearly distinguish between the monocytes of healthy, mild, and moderate disease severity. 9/
There were also significant differences in the expression of certain markers between mild and moderate COVID monocytes. Their results suggest a more profound dysfunction in moderate COVID monocytes than mild. 10/
The virus seems to impair the capacity of monocytes to activate COVID-19 virus specific CD4+ and CD8+ T-Cells and only monocytes from healthy individuals were able to trigger the activation of CD4+ specific T-cells. 11/
Monocytes from COVID-19 patients display a profound defect in pathogen sensing which is more evident in moderate patients than mild patients and showed an impairment in pro-inflammatory cytokine production and metabolic rewiring upon secondary COVID-19 stimulation. 12/
The study also found monocytes during acute infection were reprogrammed from innate immune functions to those that activate platelets and form blood clots in those with moderate COVID-19. 13/
This reprogramming suggests that monocytes may contribute to COVID-19 severity by actively impacting the process of blood clot formation and reduction in innate immune functions necessary to efficient virus clearance. 14/
Researchers also found that monocytes from COVID-19 patients produced significantly less Tumor Necrosis Factor (TNF) which causes inflammation and helps fight pathogens compared to healthy individuals. 15/
Unfortunately they also found this impacted not just COVID-19 virus, but also the common cold coronaviruses and some bacteria which means it could be harder for your body to fight off secondary infections. 16/
If your monocytes were in this state when you got infected with a cold, it could help explain why so many people are having much more severe colds than usual or unable to fight off bacterial infections as easily. 17/
It is important to note that these changes in monocytes were found during acute infection, mostly in people with moderate COVID disease and they did not look at how long these changes lasted. 18/
They did find that exposing the monocytes to a secondary stimulation of COVID in the lab (outside the body) led to a diminished immune response which the authors believe are due to the metabolic defects previously discovered from the first infection. 19/
It is unknown how long monocytes may remain in a dysfunctional or reprogrammed state. 20/
Your nasal airways contain mucus which traps inhaled virus particles and other pathogens which are then swept away by ciliated (hair-like) epithelial cells providing an essential first barrier to protect from infection ( annualreviews.org ). 21/
Things get worse in winter where humidity levels drop and your nose becomes more dry. The height of the mucus layer is reduced and the cilia are more immobilized so become less effective at protecting against pathogens. 22/
A new study has found how COVID-19 virus bypasses this protection barrier and reprograms your own machinery to help replicate in the upper airways ( cell.com ). H/T: @paulseaman31 23/
While pathogens normally can't penetrate the mucus layer, COVID-19 actually evades this defense by infecting the ciliated cells which reach up into the mucus layer to keep moving particles and pathogens in one direction to be destroyed ( ). 24/
The virus doesn't directly infect the other cell types in the nasal lining (goblet, basal cells) but instead hijacks the cell machinery to greatly enlarge and branch the microvilli (blue protrusions in diagram). 25/
The modified microvilli reach back up into the mucus layer (like Jack and the Beanstalk) so the replicated virus particles can escape to eventually reach and infect other parts of the body. 26/
This allows the virus to continue moving down the respiratory tract, infecting more and more ciliated cells along the way, showing that COVID is using yet another method to bypass the normal immune defense. 27/
Researchers also found that Omicron variants bind better to these ciliated cells and show accelerated viral entry compared to older variants such as Delta. 28/
Dry air also allows virus laden aerosols to evaporate more, become smaller, and float in the air longer increasing the chance that others might breathe them in and become infected. 29/
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