Zdenek Vrozina Profile picture
Health Care Consulting

Feb 19, 14 tweets

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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