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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SARS-CoV-2 spike protein may directly amplify brain inflammation.
➡️ Researchers found that spike proteins can colocalize with amyloid-β (Aβ) and trigger distinct inflammatory responses in microglia — the brain’s immune cells.
➡️ This raises important questions about potential long-term neurodegenerative consequences of COVID-19. 1/
Researchers developed advanced “expansion microscopy” techniques that physically enlarge human brain tissue, allowing scientists to see disease-related structures at near-nanoscale resolution using ordinary microscopes. 2/
Applying this method to brains from some COVID-19 patients revealed tiny amyloid-like protein clusters closely associated with SARS-CoV-2 particles in a small subset of cases, suggesting a possible link between COVID-19, neuroinflammation, and abnormal protein aggregation in the brain.
The study highlights how ultra-high-resolution imaging could uncover previously hidden mechanisms of neurological disease. 3/
👉 The lungs may remain biologically altered long after acute infection resolves. 1/
A new review highlights how persistent immune activation in LongCOVID may lead to:
• Fibrosis-like lung changes
• Endothelial dysfunction
• Microvascular injury
• Ongoing respiratory symptoms
COVID may end clinically—but not biologically.
#LongCOVID #Pulmonology 2/
LongCOVID respiratory sequelae may result from a “perfect storm” of:
COVID-19 may be, in part, a mitochondrial disease.
➡️ A Cambridge review shows SARS-CoV-2 disrupts mitochondrial function in lung cells—driving inflammation and worsening pneumonia.
➡️ Emerging studies suggest even after the active infection is resolved, residual viral proteins, particularly SARS-CoV-2 spike protein, may linger and continue to cause damage to the mitochondria by increasing oxidative stress and disrupting energy metabolism, offering a plausible mechanism for #LongCOVID. 1/
H/T: @CatchTheBaby
COVID-19 is not just viral—it’s metabolic.
SARS-CoV-2 hijacks mitochondria →
↓ Energy production
↑ Inflammatory signaling
A key pathway worsening lung injury. 2/
Mitochondria may link acute COVID → #LongCOVID.
Viral disruption of mitochondrial function can persist, sustaining oxidative stress and immune dysregulation even after infection. 3/
New study shows SARS-CoV-2 directly damages heart cell mitochondria—key energy engines—offering a mechanistic link to #LongCOVID cardiovascular symptoms. 1/
#LongCOVID may be a mitochondrial disease: electron microscopy reveals structural damage & myofilament breakdown in cardiomyocytes. 2/
Biopsies from LongCOVID patients confirm myocarditis with mitochondrial disruption—mirrored in infected animal models. Strong biological plausibility for persistent cardiac symptoms. 3/