2) COVID-19 saw rapid SARS-CoV-2 evolution. Pre-Omicron, prior infection provided strong, lasting protection against reinfection. But Omicron changed this - recent Omicron infections only briefly protected, with protection waning quickly.
3) Researchers link this to a shift in evolutionary pressures. Initially, the virus adapted to spread more easily. But with Omicron, when many had immunity, it evolved to evade that immunity through mutations, especially in the spike protein.
4) This immune evasion explains Omicron's lack of lasting protection. Yet prior infection still strongly prevented severe disease, suggesting different immune responses protect against mild vs. severe illness.
5) This highlights SARS-CoV-2's adaptability and the need to continually monitor the virus and update vaccines to keep up with its changes.
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2) The study introduces AIR-SPACE, a method combining high-resolution spatial mapping and immune receptor sequencing. Using this, researchers studied viral infection in mouse lymph nodes and made several discoveries.
3) Early infection stages showed distinct "activation hubs" in the lymph node where immune cells produced high levels of the antiviral protein interferon-gamma. These hubs had unique gene expression patterns based on location.
How antibodies like ICO-hu104 can neutralize SARS-CoV-2, even as the virus mutates, by targeting regions of the spike protein beyond just the receptor binding domain biorxiv.org/content/10.110β¦
2) The SARS-CoV-2 virus has a spike protein that lets it infect human cells. Researchers studied an antibody called ICO-hu104 that binds to the spike protein. They found that when ICO-hu104 binds, it changes a part of the spike protein called HR1.
3) This could prevent the virus from fusing with and entering human cells. The researchers think this is how ICO-hu104 can neutralize the virus, even as it mutates.
The NASAL IMMUNE RESPONSE:
How Human Lymphoid Tissues Combat SARS-CoV-2 and Shape Lasting Immunity β Insights from Groundbreaking Biopsy Research on Adaptive Defense Mechanisms Against Viral Challenges
(Key study in Nature π―π₯) nature.com/articles/s4159β¦
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
(π§΅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/d4158β¦
Reference study : nature.com/articles/s4158β¦
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/s4159β¦
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")