SARS-CoV-2 can break immune balance - sometimes boosting our ability to neutralize the virus, other times increasing the risk of autoimmune damage.
A new study shows how autoantibodies after COVID-19 act like a double-edged sword.🧵
A new study shows how autoantibodies after COVID-19 act like a double-edged sword.🧵
Autoantibodies = antibodies that mistakenly attack the body’s own tissues (aka nuclear proteins, enzymes, or immune receptors).
They’re common in diseases like lupus.
After COVID-19, autoantibodies often appear. But what do they mean for severity and immunity?
They’re common in diseases like lupus.
After COVID-19, autoantibodies often appear. But what do they mean for severity and immunity?
Alone, no single autoantibody predicted hospitalization. But the combination of SSA/Ro52 (nuclear protein), Jo-1 (tRNA enzyme), and RNP (RNA-protein complex) showed up more often in hospitalized & ICU patients.
And paradox - some autoantibodies correlated with better neutralization of tough variants (like Beta and Delta).
Examples - RNP/Sm, PCNA (cell cycle protein), Scl-70 (DNA enzyme), PL-12 (tRNA enzyme).
More autoreactivity, stronger neutralization.
Examples - RNP/Sm, PCNA (cell cycle protein), Scl-70 (DNA enzyme), PL-12 (tRNA enzyme).
More autoreactivity, stronger neutralization.
Anti-IFNα autoantibodies (5% neutralizing, 11% binding) weren’t directly tied to severe disease.
What are they?
They target interferon-alpha - a key antiviral signal that tells cells to block virus replication.
Binding = attach to IFNα, may reduce its activity.
Neutralizing = actually block IFNα’s protective effect.
In this study, they often appeared alongside other autoantibodies - a sign of wider immune imbalance.
What are they?
They target interferon-alpha - a key antiviral signal that tells cells to block virus replication.
Binding = attach to IFNα, may reduce its activity.
Neutralizing = actually block IFNα’s protective effect.
In this study, they often appeared alongside other autoantibodies - a sign of wider immune imbalance.
In plain terms: COVID-19 can loosen the brakes of the immune system.
B cells fire on all cylinders
Strong antibodies against the virus
But also more collateral fire on self-tissues
B cells fire on all cylinders
Strong antibodies against the virus
But also more collateral fire on self-tissues
Why they link to HIV and flu?
In HIV, broadly neutralizing antibodies often arise - super potent, but frequently autoreactive.
Shows that strong neutralization and autoimmunity can be two sides of the same coin.
COVID-19 may follow this pattern.
In HIV, broadly neutralizing antibodies often arise - super potent, but frequently autoreactive.
Shows that strong neutralization and autoimmunity can be two sides of the same coin.
COVID-19 may follow this pattern.
Important nuance.
Autoantibodies ≠ always harmful by themselves.
Sometimes they’re just byproducts of an over-activated immune system.
But the more autoantibodies, the higher the biological risk of long-term issues (autoimmune diseases, long COVID).
Autoantibodies ≠ always harmful by themselves.
Sometimes they’re just byproducts of an over-activated immune system.
But the more autoantibodies, the higher the biological risk of long-term issues (autoimmune diseases, long COVID).
Limitations matter.
Only 38 patients
No uninfected controls
Age/comorbidity differences, sampling times varied
These findings are exploratory, not definitive.
Only 38 patients
No uninfected controls
Age/comorbidity differences, sampling times varied
These findings are exploratory, not definitive.
Sum:
COVID-19 - frequent autoreactivity
Combo SSA/Ro52–Jo-1–RNP linked to worse outcomes
Some autoantibodies correlate with stronger neutralization
Not proof that autoimmunity protects - correlation ≠ causation
COVID-19 - frequent autoreactivity
Combo SSA/Ro52–Jo-1–RNP linked to worse outcomes
Some autoantibodies correlate with stronger neutralization
Not proof that autoimmunity protects - correlation ≠ causation
COVID-19 doesn’t just infect. It reshapes the immune system.
Autoantibody profiles could become biomarkers for severe disease or long COVID - but we’re not there yet.
Autoantibody profiles could become biomarkers for severe disease or long COVID - but we’re not there yet.
This is a hypothesis, not a final verdict.
We need larger, longitudinal studies.
But the signal is clear - SARS-CoV-2 disrupts immune balance - sometimes helping fight the virus, sometimes turning against us.
We need larger, longitudinal studies.
But the signal is clear - SARS-CoV-2 disrupts immune balance - sometimes helping fight the virus, sometimes turning against us.
Jacob at al., Distinct circulating autoantibodies are associated with COVID-19 hospitalization and SARS-CoV-2 neutralization activity nature.com/articles/s4429…
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