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Immune profiling long COVID

A few weeks ago, ME Research UK’s Science and Research Lead, Dr Keith Geraghty, attended the annual International Association of CFS/ME conference. He summarised some of the standout talks of days 1 and 2 and days 3 and 4 of the conference.

One of the highlights was a very powerful talk by Prof. Akiko Iwasaki of Yale Medical School on the biochemical signatures of long COVID syndrome, with relevance to improving our understanding of ME/CFS.

Symptom profiles

Prof. Akiko Iwasaki

Prof. Iwasaki said that it was fairly easy to differentiate long COVID sufferers simply by examining their symptom profiles, just as ME/CFS patients can be identified and differentiated from healthy controls using screening tools such as the DePaul Symptom Questionnaire.

Long COVID and ME/CFS share some common features in that both are more common in women than in men, and both can be associated with symptoms such as fatigue, pain, sleep disturbance and post-exertional malaise (PEM). However, there are some exceptions, such as breathlessness being more prevalent in long COVID.

Prof. Iwasaki has teamed up with researchers from the Mount Sinai Hospital in New York to establish a long COVID study group, and recently published some of their results. (This paper has not yet been reviewed by experts, and so may be subject to correction before final publication.)

Immune profiles

The researchers recruited 215 participants, including those with long COVID, those without any persistent symptoms following SARS-CoV-2 infection, and healthy control subjects (some of whom had previously had SARS-CoV-2 infection).

Levels of different types of immune cells (such as lymphocytes, T cells, B cells and NK cells) were measured in each of these individuals using a technique called multidimensional immunophenotyping, and then a computer-assisted method was used to identify any potential biomarkers of long COVID.

Many of these immune cells were found to be increased in the blood of long COVID patients compared with the other groups, including cells involved in controlling anti-inflammatory activity, blood vessel function, and the immune response to viral infection.

In short, this picture points to an immune response to a viral infection; other immune cells that would indicate a bacterial-type infection were not raised. This is not a surprise given that we know these long COVID patients had been infected with SARS-CoV-2. But if such a profile were to be found in ME/CFS as well, that might indicate that ME/CFS is also the result of a viral rather than bacterial insult.

Low cortisol

Another interesting finding was that levels of free cortisol were reduced by approximately 50% in the long COVID patients. Cortisol is a hormone produced by the adrenal glands, and which controls many functions of the body, including insulin uptake, metabolism, regulation of the immune system, digestion, and the sleep cycle.

While the researchers could not explain this result, it is something we have also seen previously in ME/CFS, and may indicate adrenal fatigue or some other response to chronic infection.

What does this mean for ME/CFS?

First, highly qualified scientists at some of the world’s top research labs are taking an interest in long COVID, and, by association, ME/CFS. Prof. Iwasaki had a panel of ME/CFS advocates to advise on her studies, and she wishes to replicate her results in an ME/CFS patient cohort.

Second, the type of immune picture developing in long COVID mirrors many of the findings made in earlier ME/CFS research studies, namely activation of the immune system, most likely in response to a virus (like Epstein-Barr virus) or reactivation of latent viruses when the host is weakened by another infection.

One of the most exiting aspects of Prof. Iwasaki’s study is that this type of immune profiling, which can be used to identify and differentiate long COVID patients, may also be applicable to ME/CFS in the near future.

We may not be too far away from a blood test that can detect ME/CFS immune signatures, and from explaining the key biochemical pathways that lead to ME/CFS.

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