Getting the COVID and flu shot together?
A new Italian study in Cytokine found that the early inflammatory response after getting COVID-19 and flu vaccines at the same time may actually limit how long your antibody protection lasts🧵
29 healthcare workers received both
an mRNA COVID-19 (XBB.1.5) booster
a quadrivalent inactivated flu shot.
Blood was collected
before vaccination (T0)
5 days later (T1)
after 3 months (T2)
after 6 months (T3)
Within just 5 days, levels of inflammatory cytokines shot up -
especially IL-6, CXCL10, and TNF-α.
In some people, IL-8 also spiked and strongly correlated with IL-6.
That means their innate immune system went into high gear.
When scientists checked antibody levels later on, they found
The higher your IL-6 and IL-8 response at day 5,
the lower your anti-spike IgG at 3 and 6 months.
So - a stronger early inflammation = faster antibody decline.
This wasn’t an all-or-nothing pattern - it was continuous.
Everyone responded, but those with the highest IL-6/IL-8 bursts lost antibodies more quickly.
It’s a dose-response relationship, not a random fluke.
Why does this matter?
IL-6 and IL-8 drive short-term inflammation.
If they rise too much, they can disrupt germinal center formation -
where long-lived memory B cells are made.
You get quick antibodies … but they don’t stick around.
So, simultaneous COVID + flu vaccination might not be harmful,
but it could change the quality and persistence of the immune response.
This study isn’t about safety - it’s about immunological balance.
Sum:
n = 29 healthcare workers
IL-6 ↑ in most participants
IL-8 ↑ in ~half
Strong negative correlation between IL-6/IL-8 rise and later IgG levels
Coordinated IL-6/IL-8 response = faster antibody waning
The strength of early inflammation doesn’t just shape how strong your immune response is - it also shapes how long it lasts.
Sometimes, less inflammation means longer protection. @szupraha @ZdravkoOnline @vlvalek @adamvojtech86
Schiavoni et al., Cytokine 2025. IL-6 and IL-8 elevations after co-administration of COVID-19 and influenza vaccines are associated with lower anti-spike IgG titers at three and six months post-vaccination. sciencedirect.com/science/articl…
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Long COVID in women and men are not the same disease. They share symptoms, but diverge in biology - immune, hormonal, and genetic.
After months since the preprint -
peer-reviewed study is now out in Cell Reports Medicine.🧵
This is the complete analysis immunity, hormones, and gene expression in 78 Long COVID with ME-CFS patients.
It confirms what patients have said for years -
this condition is biological, measurable, and deeply sex-specific.
In women, the immune system never stands down.
chronic inflammation, exhausted T cells, and loss of regulatory Tregs
leaky gut - constant immune activation
high IL-6, IL-1α, TNF-α, IFN-γ
low testosterone and cortisol - hormones that normally keep inflammation in check.
It’s not overreaction. It’s immune dysregulation.
Chronic inflammation meets hormonal collapse.
A new study from Hong Kong Baptist University examined how mRNA COVID-19 vaccines might influence insulin signaling.
The finding?
The spike protein can interfere with metabolic pathways - but mainly in people with type 2 diabetes (T2D)🧵
In mice given 4 doses of the mRNA vaccine, researchers observed impaired glucose tolerance, reduced insulin sensitivity, and higher triglycerides.
At the molecular level, phosphorylation of IRβ and Akt - key insulin signaling steps - was reduced.
Liver transcriptomics showed activation of NF-κB, MAPK, and AMPK-related pathways.
A new study in The Lancet Child & Adolescent Health followed nearly 14 million children in England.
It shows that SARS-CoV-2 infection leaves long-term marks on the vascular and immune system - even in kids.
Not just for weeks, but measurable up to a year later🧵
After COVID-19, children had a sharply increased risk of
systemic inflammatory syndromes (MIS-C, etc)
venous thrombosis
thrombocytopenia
myocarditis and pericarditis
And part of these risks remained elevated 12 months post-infection.
That means - even if a child feels fine after COVID, the body may stay in a dysregulated immune and vascular state - with lingering inflammation and endothelial stress.
In biological terms, COVID leaves a footprint
New study in BMC Immunology shows that COVID-19 leaves a lasting “aka Long Covid” imprint in the immune cells of older adults. What does that mean - and why does it matter?🧵
Months after recovery, immune cells in elderly people remain abnormally prone to die - through apoptosis.
Even when the virus is long gone, the immune system still shows signs of cellular damage and exhaustion.
Researchers analyzed peripheral blood mononuclear cells (PBMCs) - the core soldiers of the immune system, including T cells and monocytes.
In post-COVID seniors, twice as many cells were apoptotic compared to healthy controls.
A experimental study in Scientific Reports shows that the SARS-CoV-2 spike protein alone can trigger an autoimmune response against the ACE2 receptor - the very receptor the virus uses to enter cells.
The mechanism mirrors tissue damage seen in severe COVID-19🧵
This study is a proof-of-concept.
When the immune system reacts to the SARS-CoV-2 spike protein, part of that response can flip into autoimmunity against ACE2, the receptor the virus normally uses to enter cells.
In other words - the immune system doesn’t just make antibodies against the spike -
it can also generate anti-idiotype antibodies (and T-cell clones) that mistakenly recognize and attack ACE2, because ACE2 structurally mirrors the very site the spike protein binds to.
A massive Swedish study on Nature Communications Medicine tracked 810,851 people after COVID.
Only 1.4% received an official post-COVID-19 condition (PCC) diagnosis - but that reflects only those who made it into the system.
Real prevalence of long COVID is many times higher🧵
Who was most likely to be diagnosed with PCC?
severe acute infection
unvaccinated status
female sex, older age
higher education, essential jobs (healthcare, teachers, drivers…)
pre-existing conditions - asthma, thrombosis, fibromyalgia, depression, anxiety, stress disorders
Biological core of the findings
Severity of acute infection
The strongest predictor by far.
The more severe the acute phase, the higher the PCC risk - stronger inflammation, higher viral load, and deeper tissue injury mean a greater chance some immune processes remain stuck on.