Zdenek Vrozina Profile picture
Feb 19 14 tweets 2 min read Read on X
This new study shows that SARS-CoV-2 can systematically reprogram cellular metabolism to support its own survival.
This isn’t just tissue damage.
It’s a redirection of the body’s energy systems🧵
This is a recent mini-review examining how COVID-19 affects lipid profiles and the metabolome, especially in people with type 2 diabetes.
By synthesizing multiple studies, the authors show that SARS-CoV-2 profoundly disrupts metabolic balance.
One consistent finding after infection?
Decreases in HDL, LDL, and total cholesterol,
variable changes in triglycerides
These shifts are not random.
They closely track with inflammation and disease severity.
Importantly, the review highlights that the virus actively interferes with metabolic pathways.
It upregulates lipid-metabolism genes such as CD36 and PPAR-γ and redirects cellular energy flows.
In simple terms - the virus repurposes host metabolism to fuel its own replication.
COVID also triggers intense oxidative stress - excessive ROS production, lipid peroxidation, formation of toxic aldehydes.
These processes damage mitochondria, blood vessels, and DNA.
A key conclusion of the review?
Metabolic disturbances can persist long after infection.
Some patients develop new dyslipidemia, worsening glucose control, and increased cardiovascular risk.
In this sense, COVID acts as a long-term metabolic stressor.
Only at first glance, this might seem like just another review of lipid changes in COVID.
But it actually points to something much more fundamental.
It is a virus that actively rewires cellular energy systems.
The review shows that infection leads to
activation of lipid-metabolism genes (CD36, PPAR-γ)
shifts in amino-acid metabolic pathways
rerouting of cellular energy toward viral replication
This pattern is typical of chronic pathogens - not of ordinary respiratory viruses.
Falling cholesterol is not a good sign.
Lower HDL and LDL are not protective in this context.
Instead, they correlate with stronger inflammation and worse outcomes.
So hypolipidemia here acts as a marker of systemic immune stress.
Oxidative stress is one of the central mechanism. This biological signature closely resembles what we see in metabolic syndrome, chronic inflammation, accelerated biological aging.
Metabolic pathways do not always return to baseline after infection.
This helps explain long-term dyslipidemia, increased diabetes risk after COVID, elevated cardiovascular risk.
In short - COVID can act as a metabolic reset toward chronic dysregulation.
Sum:
This review suggests that SARS-CoV-2 doesn’t just cause temporary metabolic changes - it can systematically reprogram cellular metabolism to support its persistence, potentially driving long-term health consequences.
Pawłuszkiewicz at al., COVID-19 Impact on Lipid Profile and Metabolome in Patients with Type 2 Diabetes Mellitus: Mini-Review. eurekaselect.com/article/153034

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More from @ZdenekVrozina

Feb 21
This pediatric long COVID study found an immune fingerprint where the authors explicitly flag parallels with chronic viral infections (they name HIV-1) not as a slogan, but as part of how they interpret their own data🧵
JCI Insight 2026. Pediatric long COVID vs kids post-infection without long COVID, sampled around ~3 months after acute infection.
We covered this topic in the preprint, now we’re going into more detail given how important it is.
What they did - deep immune phenotyping (PBMC flow cytometry) + antibody profiling (anti-RBD/S2/N IgG/IgA) + pseudovirus neutralization.
Read 24 tweets
Feb 20
After COVID and HIV (even on ART), your cells can carry a clear immune aging signature - especially inside naive CD8 T cells🧵
A new paper uses single-cell RNA-seq to ask a sharper question.
Is the aging signal coming from changed immune-cell proportions (systemic), or from aging-like shifts inside the cells themselves (intrinsic)?
The team built a T-cell aging clock called Tictock (T immune cell transcriptomic clock).
It predicts cell type + transcriptomic age across 6 T-cell subsets.
Read 16 tweets
Feb 20
SARS-CoV-2 in brain tumors - what does it actually mean?
A new study analyzed brain tumor samples from 72 COVID-19 patients (Omicron BA.5 wave) to see whether the virus can be found directly inside tumors - and how it affects their immune environment🧵
First - nothing mystical here.
Tumors are still tissue. They often have abnormal vessels, disrupted barriers, and altered immunity.
So the real question isn’t can virus be there? - but what happens if it is.
Why might viral components be found in tumors at all?
Tumors have leaky, abnormal blood vessels and impaired drainage (EPR effect), and brain tumors often disrupt the blood-brain barrier.
This allows viruses, proteins, and immune complexes circulating in blood to more easily enter and persist within tumor tissue.
Read 16 tweets
Feb 19
Even three years post-infection, a subset of COVID survivors shows a persistently altered immune landscape, marked by elevated cytokines and incomplete recovery of key immune cell populations.🧵
Some inflammatory signals remain elevated, and certain immune cell populations never normalize. The strongest and most consistent changes involve the T-cell compartment rather than innate immune cells.
The authors describe the pattern as resembling immunosenescence because
naive CD4 and CD8 T cells - the reserve needed to respond to new infections - remain persistently reduced.
Read 21 tweets
Feb 18
Researchers looked at markers of cellular and mitochondrial damage in the blood of people with Long COVID and linked them to cognition, psychological distress, and inflammation. They identified several surprising associations🧵
Finding 1. Long COVID = lower relative ccf-mtDNA
At first glance, this is surprising.
People usually expect - mitochondrial damage - more mtDNA released into blood.
But here, researchers found lower relative levels.
But this does not necessarily mean less damage.
It likely reflects dysregulation of mitochondrial quality control (mitophagy).
Read 14 tweets
Feb 17
One of the most important recent studies on post-COVID biology delivers a concerning message.
SARS-CoV-2 doesn’t just affect immune cells.
It can leave long-lasting changes directly in the immune proteins circulating in our blood.🧵
Think of the immune system in three layers.
immune cells (T, B, NK…)
signaling molecules
effector proteins - antibodies and complement
This study shows persistent changes in the deepest layer - the effector proteins themselves.
Researchers analyzed blood samples from more than 400 people after COVID-19.
They identified hundreds of chemical alterations in proteins - called ncAA modifications.
It’s about proteins becoming chemically different.
Read 14 tweets

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