Autoantibodies In Covid-19

This post is based on the Guardian article “Autoantibodies may be driving severe Covid cases, study shows” which some of you have kindly sent through to me; and "SARS-CoV-2, the autoimmune virus" in

What are autoantibodies?

Antibodies are proteins that are released by the cells of the immune system. They disable viruses by latching on to their surface proteins and preventing them gaining access to the body’s cells.

Autoantibodies are antibodies that attack the body itself by mistake and disrupt the normal function as a result.

This is often referred to as “friendly fire” as your are being attacked my something that should be protecting you. Autoantibodies can be made and triggered by the SARS-CoV-2 virus. The autoantibodies attack and this results in:

  1. The blocking of our antiviral defences

  2. The destroying of helpful immune cells,

  3. The body's organs being attacked- from the brain, blood vessels, lung, heart, to the gastrointestinal tract.

  4. Susceptibility to the infection

In a recent study it found that more than 5% of hospitalised patients had autoantibodies that weakened a key arm of the immune defence which uses proteins called interferons. These patients were unable to control the amount of virus in their bodies and so developed a more serious illness. Other patients had autoantibodies that targeted B cells, the cellular factories that churn out antibodies to fight the virus. One patient had autoantibodies that appeared to wipe out many of their protective T-cells.

This demonstrates how autoantibodies might have a pivotal role in the severity and life-threatening manifestations in COVID-19 patients.

In a recent flurry of research studies there seems to be a strong association between severe SARS-CoV-2 infection and autoimmunity.

Autoimmune disease proved to be secondary to COVID-19 infection:

Guillain-Barré syndrome - Anti-nuclear antibodies (ANA)

Miler Fisher Syndrome (MFS) - Anti-cardiolipin (aCL) antibodies

Antiphospholipid syndrome - Anti-β2 glycoprotein 1 (aβ2GP1) antibodies

Immune thrombocytopaenic purpura - Anti-MDA5 antibodies

Systemic Lupus Erythematosus (SLE) - Anti RBC antibodies (direct anti globulin)

Kawasaki disease - LAC –lupus anticoagulant

Cold agglutinin disease & autoimmune hemolytic anemia - Antiprothrombin IgM

Neuromyelitis optica - Antiphosphatidylserine IgM/IgG

NMDA-receptor encephalitis - Antiannexin V IgM/IgG

Myasthenia gravis - Anti-GD1b antibodies

Type I diabetes Anti-heparin PF4 complex antibody

Large vessel vasculitis & thrombosis - pANCA AND cANCA

Psoriasis - Anti-CCP antibodies

Subacute thyroiditis

Graves' disease


Inflammatory arthritis

Latest Autoantibodies to be identified in acute Covid-19:

Rather than one type of autoantibody being to blame, researchers believe that Covid-19 is worsened when many different antibodies arise in the same patient such as

  • Anti-nuclear antibodies

  • Lupus anti-coagulant

  • Anti-SSA/Ro antibodies

  • Antiphospholipid antibodies

  • Anti-IFN antibodies

  • Anti-MDA5 antibodies

  • Anti-Angiotensin-converting enzyme 2 (ACE2) autoantibodies

But autoantibodies are not the whole story. It is very likely our genetics play a part too.

The human leukocyte antigen (HLA) gene and its different genetic variants are already know to be associated with the development of various autoimmune diseases. So it is not that surprising that there is a strong association between covid-19 and HLA genetic variants. For more on genetic susceptibility to Covid-19 please see my post "Genetics and Covid"

A current working hypothesis is that the SARS- CoV-2 virus attacks and those patients who are genetically susceptible (such as HLA- DRB1) then have hyperstimulation of the immune system with fever, high levels of ferritin and production of autoantibodies. This results in a severe Covid -19 infection with autoimmune disease sequelae.

Autoantibodies and Long Covid:

Autoantibodies may cause medical conditions in Covid-19 patients long after the virus itself has been beaten

So if the an acute covid-19 infection’s severity is a result of a genetic / autoantibody interplay it may be that these harmful effects continue after the infection has abated, leaving patients with longer-lasting medical problems i.e. Long Covid. It is known that autoantibodies can persist for a very long time so presumably they can keep on damaging for a very long time ?

There is growing evidence that those with Long Covid are suddenly finding themselves with inflammatory arthritis, myasthenia gravis, subacute thyroiditis and diabetes. I am encouraged to see that researchers are firstly acknowledging Long Covid and secondly starting to look at how our genetic make up and subsequent production of autoantibodies during the acute stage of a Covid-19 infection may in some way explain why we too are still suffering from the long term affects of a “viral illness that in most will only last two weeks”.

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