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Immunological dysfunction persists for 8 months following initial mild-moderate SARS-CoV-2 infection, 2021, Phetsouphanh et al

Discussion in 'Health News and Research unrelated to ME/CFS' started by strategist, Jun 8, 2021.

  1. strategist

    strategist Senior Member (Voting Rights)

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    Preprint

    Abstract

    A proportion of patients surviving acute COVID-19 infection develop post-COVID syndrome (long COVID) encompassing physical and neuropsychiatric symptoms lasting longer than 12 weeks. Here we studied a prospective cohort of individuals with long COVID (the ADAPT study) compared to age/gender matched subjects without long COVID, healthy donors and individuals infected with other non-SARS CoV2 human coronaviruses (the ADAPT-C study). We found an elevated diffuse serum inflammatory cytokine profile in symptomatic long COVID subjects that was maintained at 8 months post-infection and was not observed in asymptomatic COVID-19 survivors. This inflammatory profile consisted of 15 cytokines that positively correlated; revealing an apparent diffuse, potentially coordinated, low level up regulation of a spectrum of immune and inflammatory mediators. In addition, we found an absence of subsets of un-activated naїve T and B cells in peripheral blood of long COVID subjects, that did not reconstitute over time. In contrast, individual serum cytokines from the interferon I and III classes, T cell activation markers and plasma ACE2, while elevated in the serum of people previously infected with SARS-CoV-2 were not further elevated in subjects with long COVID symptoms. This work defines immunological parameters associated with long COVID and suggests future opportunities to prevention and treatment.

    https://www.medrxiv.org/content/10.1101/2021.06.01.21257759v1

    The missing T and B cell subsets

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    Last edited by a moderator: Jun 10, 2021
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  2. Andy

    Andy Committee Member (& Outreach when energy allows)

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    "Our data does have some limitations. Firstly, although our long COVID ‘cases’ and controls were matched for two major characteristics (age and gender) it is possible that the differences observed reflect other key demographic or other factors between the groups. Secondly, although 7 of the 29 analytes were observed to be abnormally elevated, 22 of 29 were not (including key cytokines often implicated in chronic fatigue syndromes such as Pentraxin- 3(PTX3), TGF-β1, and IL-13)62,63. This suggests long COVID may be differentiated from other post viral fatigue syndromes, however, our results require validation in other cohorts of long COVID to ensure their replicability."

    Those references are

    62. Tomoda, A., et al. Cytokine production and modulation: comparison of patients with chronic fatigue syndrome and normal controls. Psychiatry Res 134, 101–104 (2005)
    63. Montoya, J.G., et al. Cytokine signature associated with disease severity in chronic fatigue syndrome patients. Proc Natl Acad Sci U S A 114, E7150–E7158 (2017).

    which seems like it is a limited selection.
     
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  3. Hutan

    Hutan Moderator Staff Member

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    An Australian paper. Authors:
    1. Chansavath Phetsouphanh 1*&,
    2. David Darley 2*,
    3. Anette Howe 1,
    4. C. Mee Ling Munier 1,
    5. Sheila K Patel 3,
    6. Jenifer A Juno 4,
    7. Louise M Burrell 3,
    8. Stephen J Kent 4,5,
    9. Gregory J Dore 1,2,
    10. Anthony D Kelleher 1,2& and
    11. Gail Matthews 1,2&
    1. The Kirby institute, University of New South Wales, NSW 2033, Australia
    2. St Vincent’s Hospital, Darlinghurst, NSW 2010, Australia
    3. Department of Medicine, Austin Health, University of Melbourne, Victoria 3084, Australia
    4. Department of Microbiology and Immunology, Peter Doherty Institute, University of Melbourne, Victoria 3000, Australia
    5. Melbourne Sexual health centre, Infectious Diseases Department, Alfred health, central Clinical School, Monash University, Melbourne, Victoria 3004, Australia
    Worth noting that Professor Andrew Lloyd is the Head of the Viral Immunology Systems Program with the Kirby Institute at the University of New South Wales, which is where 6 of the 11 authors are based. Lloyd is a leading proponent of BPS thinking, especially as applied to ME/CFS. Given the subject of the paper, he will have certainly had an influence. So it's interesting to see the suggestion that Long Covid is something other than CFS coming from this group, as well as the ongoing efforts in cytokine measurements. Positioning Long Covid as different to CFS allows them to continue to easily maintain that GET and CBT fix CFS, while winning funding to investigate the biological basis of Long Covid.
    Lloyd is also the head of the UNSW Fatigue Clinic and Research Program.

    Austin Health has been on our radar as a hotbed of MUS thinking in Melbourne. 2 of the 11 authors are with Austin Health, although they may not be associated with the MUS part - I haven't looked.
     
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