➡️ 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/
A new review highlights how neurotropic viruses like SARS-CoV-2 reprogram the metabolism of brain immune cells — especially microglia and astrocytes — contributing to neuroinflammation and brain dysfunction.
➡️ Under normal conditions, glial cells use oxidative phosphorylation (OXPHOS) to support brain homeostasis and anti-inflammatory functions. But viral infection shifts them toward aerobic glycolysis, driving pro-inflammatory cytokine production and immune activation. 1/
This metabolic switch:
• increases inflammatory mediators (IL-1β, TNF-α)
• elevates oxidative stress
• impairs neuronal support
• disrupts the blood-brain barrier
All of which can exacerbate neuroinflammation and damage. 2/
For SARS-CoV-2 specifically, the viral S1 protein can cross the BBB and trigger microglial activation and inflammasome (NLRP3) signaling, which further promotes inflammation and potentially persistent neurological effects. 3/
Breakthrough in respiratory virus prevention (Flu, COVID & more)
➡️ Researchers have developed an AI-designed intranasal antiviral platform that could block multiple respiratory viruses—flu, COVID-19, and future variants—right at the entry point: the nose. 1/
The platform is based on interferon-lambda, a natural antiviral protein, redesigned using AI protein engineering to overcome major limitations: poor heat stability and rapid clearance from nasal mucosa.
➡️ Using AI, scientists strengthened unstable protein regions, improved solubility, and added glycoengineering—making the protein so robust it remained stable for 2 weeks at 50 °C. 2/
To keep it in the nose longer, the protein was packaged in nanoliposomes and coated with chitosan, greatly improving adhesion to nasal mucosa and penetration through thick mucus. 3/
New study in International Journal of Infectious Diseases highlights persistent immune alterations after SARS-CoV-2 infection—providing further biological evidence for #LongCOVID as a genuine post-infectious condition.
➡️ Researchers found lasting changes in immune activation and regulation, even months after recovery from acute COVID-19—suggesting the immune system does not fully reset after infection. 1/
Key findings point to chronic inflammation, altered cytokine responses, and immune imbalance, which may explain prolonged symptoms such as fatigue, pain, and neurocognitive complaints.
➡️ Importantly, these immune changes were seen independent of initial disease severity, reinforcing that even mild COVID-19 can have long-term immunological consequences. 2/
The study of >40,000 people shows that key immune cells (T cells, B cells, NK cells) dropped during widespread COVID infection and stayed below pre-pandemic levels for nearly 2 years. 3/
A new Israeli study demonstrates why some people develop #LongCOVID.
➡️ By analysing immune responses, gene expression and plasma proteins in blood samples, scientists found that people with longCOVID show persistent chronic inflammation and disrupted immune signalling months after infection — patterns not seen in those who fully recovered. 1/
These immune differences help explain lingering symptoms — such as fatigue, brain fog and breathlessness — and point to specific inflammatory pathways that could be targeted for treatment. This work opens new avenues for better therapies for millions living with longCOVID. 2/
Researchers performed immunological, virological, transcriptomic and proteomic analyses from a cohort of 142 individuals between 2020 and 2021, including uninfected controls (n = 35), acutely infected individuals (n = 54), convalescent controls (n = 24) and patients with LC (n = 28).
➡️ The LC group was characterized by persistent immune activation and proinflammatory responses for more than 180 days after initial infection compared with convalescent controls, including upregulation of JAK-STAT, interleukin-6, complement, metabolism and T cell exhaustion pathways.
➡️ Similar findings were observed in a second cohort enrolled between 2023 and 2024, including convalescent controls (n = 20) and patients with LC (n = 18). 3/
Can past COVID-19 weaken the body’s ability to fight tuberculosis?
➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/
Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).
➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/
Key finding:
➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.
➡️ Suggests prolonged immune downregulation after COVID-19. 3/
A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/
Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.
➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.
In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.
➡️ Flu does not drive the same long-term immune activation. 3/