Which arm is crucial for viral clearance & protection against #SARSCoV2? 1/
Early on in the #pandemic questions arose regarding how #SARSCoV2 is cleared during acute/primary infection & what aspects of the #adaptive immune were necessary and sufficient for protection from repeat infection 2/
Using mouse models of SARSCoV2,@BenIsraelow Rt al demonstrate that both humoral and cellular adaptive immunity contributes to viral clearance in the setting of primary infection 3/
Either convalescent mice, or mice that receive #mRNA vaccination are protected from both homologous infection & infection with a VOC, B.1.351 4/
Additionally, they conclude that protection is largely mediated by antibody response and not cellular immunity, and highlight the in vivo protective capacity of antibodies generated to both vaccine & natural infection @VirusesImmunity@SaadOmer3 5/
Another study on Rhesus #Macaques finds that T cells play a role in the recovery from acute #SARSCoV2 infections, their depletion does not induce severe disease, & T cells do not account for the natural resistance of rhesus macaques to severe #COVID19@fitterhappierAJ 6/
Neither primed CD4+ or CD8+ T cells appeared critical for immunoglobulin class switching, the development of immunological memory or protection from a second infection 7/
CD4, CD8, & CD4/8 depletion in Macaques prior and during infection did not affect disease course and only mildy attenuated viral clearance! 8/
The debate continues.....Difficult to write-off the importance of T-cells. This virus is weird. Need more studies before we dump cellular arm. What we know, a harmony between the two is needed for a successful immune response! 9/
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➡️ Compared with healthy controls,
✔ Long COVID patients had blunted morning cortisol peaks
✔ Higher evening cortisol
✔ Loss of normal circadian pattern
Blood cortisol alone failed to detect these changes. 2/
Key insight:
➡️ Salivary cortisol profiling may be a more sensitive marker of stress-system dysfunction in LongCOVID than standard blood tests.
➡️ HPA axis disruption could underlie:
• Fatigue
• Brain fog
• Sleep disturbance
• Dysautonomia. 3/
➡️ New review highlights that persistent cognitive symptoms in COVID survivors are strongly linked to pro-inflammatory cytokines and blood–brain barrier (BBB) dysfunction.
➡️ Key culprits include IL-6, TNF-α, IL-1β, IL-8, IL-13 and MCP-1 — many remain elevated months after infection.
🔥 COVID-19 is not just a respiratory disease.
➡️ Evidence suggests cognitive impairment can occur due to:
Post-COVID fatigue isn’t just subjective.
Using advanced MRI, researchers found real changes in brain blood flow and oxygen metabolism in people with Post-COVID-19 Syndrome (PCS) after mild infection.
➡️ Key finding:
PCS patients showed increased oxygen metabolism in the hippocampus (memory hub) but reduced metabolism in the anterior cingulate cortex (ACC) — despite no visible brain atrophy. 1/
Why this matters:
➡️ Higher hippocampal metabolism was linked to better cognitive performance, suggesting a compensatory response to maintain thinking and memory in PCS. 2/
In contrast, lower anterior cingulate cortex (ACC) metabolism correlated with:
Why do some people feel exhausted long after COVID-19?
➡️ New brain-imaging research shows that even after mild COVID, people with persistent fatigue can have subtle but real changes in brain structure.
➡️ These changes are not large or widespread, but tend to appear in connected brain networks, especially areas involved in attention, decision-making, and sensory processing. 1/
Importantly, the brain regions affected overlap with areas that naturally express TMPRSS2, a protein that helps SARS-CoV-2 enter cells — suggesting certain brain circuits may be more vulnerable to the virus. 2/
The study also links these changes to brain chemical systems involved in mood, energy, and cognition (serotonin, acetylcholine, glutamate, and cannabinoids). 3/
COVID-19 doesn’t just affect the lungs — it can disrupt how cells produce energy. New research shows that COVID-19 alters the genetic “switches” that control mitochondria, the structures that power our cells. 1/
By comparing people who died from severe COVID-19, those who recovered, and healthy individuals, researchers found lasting changes in how mitochondrial genes are regulated. These changes were most prominent in genes involved in energy production and metabolism. 2/
Importantly, people with COVID-19 showed abnormally high levels of proteins that control mitochondrial structure and stress responses, suggesting long-term damage to the cell’s energy system. 3/