Tired months after COVID?
A study found that even 11 months later, many people still show impaired mitochondrial function in their immune cells - a possible driver of long COVID symptoms.
And yes, even after mild infections.🧵
A study found that even 11 months later, many people still show impaired mitochondrial function in their immune cells - a possible driver of long COVID symptoms.
And yes, even after mild infections.🧵
Researchers measured mitochondrial membrane potential (ΔΨm) - a key indicator of cellular energy - in blood immune cells (PBMCs) from:
healthy controls
people with active COVID
recovered after 40 days (R1)
recovered after 11 months (R2)
healthy controls
people with active COVID
recovered after 40 days (R1)
recovered after 11 months (R2)
The result?
ΔΨm was significantly reduced in all COVID groups - including R2, 11 months post-infection.
This suggests long-lasting mitochondrial stress, even after "mild" cases with no hospitalization.
ΔΨm was significantly reduced in all COVID groups - including R2, 11 months post-infection.
This suggests long-lasting mitochondrial stress, even after "mild" cases with no hospitalization.
So why does ΔΨm matter?
It’s the voltage across the mitochondrial membrane.
If it's lost:
energy (ATP) drops
oxidative stress rises
the cell may trigger apoptosis
In short - the cell is exhausted.
It’s the voltage across the mitochondrial membrane.
If it's lost:
energy (ATP) drops
oxidative stress rises
the cell may trigger apoptosis
In short - the cell is exhausted.
Long COVID symptoms were common in the R2 group:
85% had persistent issues like fatigue, insomnia, brain fog, shortness of breath, or muscle pain.
Their immune cells still showed reduced ΔΨm - even 11 months later.
85% had persistent issues like fatigue, insomnia, brain fog, shortness of breath, or muscle pain.
Their immune cells still showed reduced ΔΨm - even 11 months later.
But - there was a striking sex difference:
ΔΨm recovered in men, but remained low in women
100% of women in R2 had ≥5 long COVID symptoms
Only 58% of men had symptoms (usually just 1-2)
ΔΨm recovered in men, but remained low in women
100% of women in R2 had ≥5 long COVID symptoms
Only 58% of men had symptoms (usually just 1-2)
The study suggests that women may experience prolonged mitochondrial stress, possibly due to hormonal or immune factors.
Meanwhile, men’s immune cells showed a partial or full recovery of mitochondrial potential.
Meanwhile, men’s immune cells showed a partial or full recovery of mitochondrial potential.
Why does this matter?
The authors link sustained ΔΨm loss to:
neurodegenerative risk (eg Alzheimer’s, Parkinson’s)
impaired recovery
chronic inflammation
Mitochondria are central to long-term health - especially in neurons and immune cells.
The authors link sustained ΔΨm loss to:
neurodegenerative risk (eg Alzheimer’s, Parkinson’s)
impaired recovery
chronic inflammation
Mitochondria are central to long-term health - especially in neurons and immune cells.
Sound familiar?
Loss of ΔΨm also happens in:
T cells with exhaustion phenotype
ROS-producing monocytes
HIV-induced immune dysfunction
SARS-CoV-2 may trigger a similar metabolic exhaustion of leukocytes.
Loss of ΔΨm also happens in:
T cells with exhaustion phenotype
ROS-producing monocytes
HIV-induced immune dysfunction
SARS-CoV-2 may trigger a similar metabolic exhaustion of leukocytes.
And while ΔΨm recovery in men looks good - it's only part of the story.
This study didn’t measure ATP production, ROS levels, or mitochondrial biogenesis.
So even recovered cells may still carry hidden dysfunction.
This study didn’t measure ATP production, ROS levels, or mitochondrial biogenesis.
So even recovered cells may still carry hidden dysfunction.
Takeaway:
ΔΨm loss might be an early biomarker for long COVID risk, a marker of energetic and immunological exhaustion.
SARS-CoV-2 may induce long-term metabolic exhaustion of leukocytes, contributing to chronic inflammation and impaired healing.
Not even a year later.
ΔΨm loss might be an early biomarker for long COVID risk, a marker of energetic and immunological exhaustion.
SARS-CoV-2 may induce long-term metabolic exhaustion of leukocytes, contributing to chronic inflammation and impaired healing.
Not even a year later.
This was an in vivo human study (n=105), using PBMCs analyzed ex vivo.
Conducted in Mexico before mid-2021 - likely pre-Delta variants (Wuhan/Alpha).
Peer-reviewed, published in Journal of Leukocyte Biology (2022).
Conducted in Mexico before mid-2021 - likely pre-Delta variants (Wuhan/Alpha).
Peer-reviewed, published in Journal of Leukocyte Biology (2022).
Díaz-Resendiz at al., Loss of mitochondrial membrane potential (ΔΨm) in leucocytes as post-COVID-19 sequelae. academic.oup.com/jleukbio/artic…
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