Preprint Identification of soluble biomarkers that associate with distinct manifestations of long COVID, 2024, Buggert et al

Discussion in 'Long Covid research' started by forestglip, Nov 11, 2024.

  1. forestglip

    forestglip Senior Member (Voting Rights)

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    Identification of soluble biomarkers that associate with distinct manifestations of long COVID

    Marcus Buggert, Yu Gao, Curtis Cai, Sarah Adamo, Elsa Biteus, Habiba Kamal, Lena Dager, Kelly Miners, Sian Llewellyn-Lacey, Kristin Ladell, Pragati Sabberwal, Kirsten Bentley, Jinghua Wu, Mily Akhirunnesa, Samantha Jones, Per Julin, Christer Lidman, Richard Stanton, Helen Davies, Soo Aleman, David Price, Paul Goepfert, Steven Deeks, Michael Peluso

    Abstract
    Long COVID is a heterogeneous clinical syndrome of uncertain etiology triggered by infection with SARS-CoV-2. We employed ultrasensitive approaches to profile the immune system and plasma proteome in healthy convalescent individuals and patients with long COVID.

    Symptomatic disease was not consistently associated with quantitative differences in immune cell lineage composition or antiviral T cell immunity. Healthy convalescent individuals nonetheless exhibited higher titers of neutralizing antibodies against SARS-CoV-2 than patients with long COVID, and extensive phenotypic analyses revealed a subtle increase in the expression of some coinhibitory receptors, most notably PD-1 and TIM-3, among SARS-CoV-2 nonspike-specific CD8+ T cells in patients with long COVID.

    We further identified a plasma biomarker signature of disease linking breathlessness with apoptotic inflammatory networks centered on the hub protein TRAF2 and dysregulated pathways associated with lung injury, cell cycle progression, and platelet activation, which could potentially inform the diagnosis and treatment of long COVID.

    Link | PDF (Preprint)
     
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  2. Hutan

    Hutan Moderator Staff Member

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    From another study:
    Improvement of immune dysregulation in individuals with long COVID at 24-months following SARS-CoV-2 infection, Matthews et al, 2024
    It also found increased PD-1 and TIM3 expression (but higher rather than lower specific antibody levels) in the Long Covid group.

    It looks like heterogeneity was a problem in this study. I wish researchers would do more sorting of potential participants on obvious symptom differences before they do their studies.
     
    Last edited: Nov 11, 2024
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  3. forestglip

    forestglip Senior Member (Voting Rights)

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    HAVCR2 (TIM-3) on Wikipedia

    The page also lists some ligands that bind to TIM-3, a couple of which rang a bell.

    It lists CEACAM1. We've seen upregulation of CEACAM3, though I'm not sure how related they are.
    Edit: CEACAM1 was upregulated in long COVID but not ME/CFS in the quoted post. CEACAM3 was upregulated in both conditions.
     
    Last edited: Nov 11, 2024
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  4. forestglip

    forestglip Senior Member (Voting Rights)

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    From reference 41 in Wikipedia page above:

    Cooperation of Tim-3 and PD-1 in CD8 T-cell exhaustion during chronic viral infection, 2010, Hyun-Tak Jin et al
    pnas.1009731107fig05.jpg
     
    Last edited: Nov 11, 2024
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  5. Sean

    Sean Moderator Staff Member

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    Heterogeneity is going to remain a significant confounder until we get some good biomarkers to help reveal any sub-groups and generally clarify diagnostic criteria.
     
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  6. Hutan

    Hutan Moderator Staff Member

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    For sure, but there are things that can be done to make more homogeneous cohorts e.g. people whose collection of symptoms meet ME/CFS criteria and who have had the symptoms for over one year; people with observable lung damage; people who were on mechanical ventilation and have observable lung damage...
     
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  7. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    It doesn't read as if these particular cohorts were hospitalised / ventilated or had observable lung damage.

     
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