When "Mr SARS-COV-2" 🤢 meets "Mrs INFLUENZA" 🥶 (1st part)
This is a fascinating subject because we sometimes see, COVID-19 which seems blocking the progression of respiratory diseases, or sometimes giving the impression of contributing to their development. What about it?
2) In a first study, Japanese researchers investigated the impact of COVID-19 on influenza activity.
They compared the number of cases positive for COVID-19 and for influenza across 22 representative countries. onlinelibrary.wiley.com/doi/10.1111/ir…
3) Theirs results demonstrate alternating prevalence of SARS-CoV-2 and influenza virus.
4) In this 2nd study, researchers showed that during simultaneous infection, SARS-CoV-2 interferes with RSV-A2 but not with A(H1N1)pdm09 replication. The prior infection of nasal airway epithelium with SARS-CoV-2 ... mdpi.com/1999-4915/14/2…
5) ... reduces the replication kinetics of both respiratory viruses. SARS-CoV-2 replication is decreased by a prior infection with A(H1N1)pdm09 but not with RSV-A2.
6) In this 3rd study, researchers explained that "a likely mechanism is the interferon response that could confer a temporary nonspecific immunity to the host." pubmed.ncbi.nlm.nih.gov/35075991/
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The NASAL IMMUNE RESPONSE:
How Human Lymphoid Tissues Combat SARS-CoV-2 and Shape Lasting Immunity – Insights from Groundbreaking Biopsy Research on Adaptive Defense Mechanisms Against Viral Challenges
(Key study in Nature 💯💥) nature.com/articles/s4159…
2) The study looks at how the immune system in the nose reacts to the SARS-CoV-2 virus, which causes COVID-19. Researchers took small tissue samples from the nasal area to see how immune cells respond during infection and recovery.
3) They found that certain immune cells, like monocytes and macrophages, help protect and repair the tissue. B cells, which make antibodies, showed strong antiviral activity.
BATTLEGROUND WITHIN:
How CANCER CELLS and SARS-CoV-2 DISRUPT MITOCHONDRIAL FUNCTION to Undermine Immune Defense
(🧵mega-thread with articles, reviews and studies)
In a recent review, they show that Cancer cells can undermine the immune system ...
2) ... by transferring defective mitochondria to T cells, reducing their cancer-fighting abilities. This challenges the belief that mitochondria remain with their original cells.
Article : nature.com/articles/d4158…
Reference study : nature.com/articles/s4158…
3) While SARS-CoV-2 does not "poison" the immune system in the same manner as cancer cells with tainted mitochondria, it does interfere with mitochondrial function, which can compromise immune responses and contribute to disease severity.
Here are latest research in this area
OUTSMARTING IMMUNITY:
How SARS-CoV-2 EVADES T CELLS in a FIGHT for SURVIVAL
Two new and amazing studies in Nature. Thanks to @DavidJoffe64
2) SARS-CoV-2 is trying to escape to T cells because these immune fighters are crucial in controlling infections.
3) The first study highlighted that robust virus-specific T cells in the lungs of COVID-19 patients effectively reduce viral loads and improve respiratory health. nature.com/articles/s4159…
2) The COVID-19 virus can trigger a severe immune reaction called sepsis, which leads to organ failure and death. Systems biology research has found that the molecular changes in severe COVID-19 are very similar to those seen in sepsis from other causes.
3) This suggests the COVID-19 virus itself, rather than just secondary infections, is directly driving the sepsis-like immune dysfunction in some patients. Additionally, the long-term effects of both severe COVID-19 (called "long COVID") and sepsis (called "post-sepsis syndrome")
SARS-CoV-2 Spike Protein Drives Harmful Fusions in Blood Vessel Cells, Potentially Worsening COVID-19 Complications
The Role of Viral-Induced Syncytia in Endothelial Cells
Thanks to @atranscendedman nature.com/articles/s4159…
2) The SARS-CoV-2 virus can make lung cells fuse together, forming large cells called syncytia. Surprisingly, the virus's spike protein can also cause this in cells that line blood vessels (endothelial cells).
3) This is important because endothelial cell problems are linked to severe COVID-19 symptoms. The researchers found that a specific enzyme, myosin light chain kinase, is needed for these syncytia to form. Cells grown on stiffer surfaces were more likely to form syncytia.