French Scientists Discover That Omicron Triggers Alarming New Immune Reactions Compared to Delta!
Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 19, 2025 1 hour, 34 minutes ago
Medical News: A Shift in the Body’s First Line of Defense
A groundbreaking study from Université Paris Cité and collaborating institutions has uncovered how different SARS-CoV-2 variants spark dramatically different responses in the immune system. Researchers focused on plasmacytoid pre-dendritic cells (pDCs)—specialized defenders that detect viruses early and sound the alarm. Surprisingly, they discovered that while Delta and Alpha variants drive strong interferon-based antiviral defenses, Omicron appears to bypass this system and instead pushes the body toward a pro-inflammatory pathway. This finding, highlighted in this
Medical News report, may help explain why Omicron spreads more rapidly but often leads to less severe illness than earlier variants.
The Immune Switch Between Delta and Omicron
When exposed to Delta, pDCs produced high amounts of interferon-alpha and interferon-lambda, powerful proteins that block viral replication. These responses, however, can also fuel dangerous “cytokine storms” if left uncontrolled. Omicron, by contrast, dampened this interferon surge. Instead, it activated the P3-pDC subset, a type of immune cell geared toward stimulating T cells and releasing inflammatory molecules like IL-6, IL-8, and TNF-alpha. The shift indicates Omicron has evolved strategies to evade early antiviral defenses while still triggering inflammation that could contribute to long-term complications.
Stronger T Cell Activation Under Omicron
The study also revealed that Omicron-exposed pDCs were far more effective at priming naïve CD4+ T cells than those stimulated by Delta. This suggests that Omicron’s tactics favor immune activation geared toward adaptive responses rather than direct antiviral action. While this could mean fewer life-threatening cytokine storms compared to earlier strains, the heightened T cell priming might also play a role in persistent post-COVID complications.
Why This Matters for Future Variants
Understanding these differences is vital as new SARS-CoV-2 variants continue to emerge. If certain variants lean toward stronger interferon production, patients could face higher risks of severe inflammatory disease. Others, like Omicron, may enhance viral spread by reducing interferon activity while skewing immune responses toward inflammation and T cell overactivation. These discoveries could influence how future therapies are designed, from interferon-based treatments to drugs that limit dangerous inflammatory pathways.
A Deeper Look Ahead
The findings emphasize that not all variants are created equal—each carries its own blueprint for manipulating the immune system. By learning how these pathways shift, researchers hope to predict which future variants might be more transmissible, more inflammatory, or more dangerous. While Omicron may appear milder on the surface, the long-term risks tied to its unique immune manipulation remain an open question. The study serves as a reminder that COVID-19 continues to evolve in ways that challenge medical science and public health worldwide.
This research is an urgent call for continued vigilance, as the virus shows a remarkable ability to exploit immune pathways differently with each new form. Understanding these mechanisms could help the world prepare not only for the next variant of concern
but also for strategies that might prevent severe disease and long-term complications.
The study findings were published in the peer reviewed journal: iScience.
https://www.sciencedirect.com/science/article/pii/S2589004225016554
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Medical News.
Read Also:
https://www.thailandmedical.news/news/scientists-discover-that-omicron-sub-lineages-use-heparan-sulfate-to-infect-cells-with-low-ace-2
https://www.thailandmedical.news/news/omicron-variant-could-signal-dangerous-shift-in-covid-19-virus-behavior
https://www.thailandmedical.news/news/study-reveals-neurological-dangers-of-mild-omicron-subvariants
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