➡️ Acrux XBB.2.3 was first spotted in India (Karnataka) & then in the USA—origin is somewhat unclear.
Here is the animated map by @Mike_Honey_ showing the spread of the XBB.2.3.* "Acrux" variant around the world. 2/
➡️ Singapore (26%) and India (22%) are still the hotspots.
Spain (11%) and Australia (8%) are also showing recent growth.
Spotted in many other countries including Japan, South Korea, China, the UK & the US. 3/
Though it is present in China & Japan, but still trying to find its way through some other dominant XBBs like XBB.1.5, XBB.1.16, XBB.1.9 etc 4/
➡️ #Acrux is evolving fast in to many offsprings, and one of its descendants, XBB.2.3.2 is considered to be the fastest.
According to @LongDesertTrain, XBB.2.3.2 also has an interesting mute ORF1a:R2159W (NSP3_R1341W) that has shown up in several fast-growing lineages 5/
➡️ In India, the share of #Acrux XBB.2.3 is increasing, but still it is not able to outcompete currently dominant #Arcturus. However, its offspring XBB.2.3.2 may have some edge over it 6/
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/