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Background: <p>Long COVID is a complex condition where symptoms persist for more than 3 months after SARS-CoV-2 infection and affects an estimated 5-30% of individuals. While persistent inflammation has emerged as an important feature of this condition, it is unclear if immune responses from COVID-19 vaccination or SARS-CoV-2 re-infection exacerbate or mirror the initial inflammatory responses.</p> Methods: <p>We quantified 182 inflammatory and neurology-related proteins in plasma using multiplexed affinity proteomics. Plasma samples from the COVID PROFILE cohort conducted in Victoria, Australia, were collected 6-9 months after first infection, but before COVID-19 vaccination from individuals who had recovered from COVID-19 (<i>n</i> = 21) or from individuals with long COVID (<i>n</i> = 12). To establish baseline plasma profiles, protein levels were benchmarked against unvaccinated, SARS-CoV-2 naive individuals (<i>n</i> = 24). In addition, we performed longitudinal analysis in a subset of individuals (<i>n</i> = 34), where paired samples collected 2-4 weeks after a third COVID-19 vaccine dose and after SARS-CoV-2 breakthrough infection were available to assess inflammatory and neurology protein plasma levels after antigen exposure in these contexts.</p> Results: <p>In this cohort Boruta feature selection and lasso regression models identified IL-20, HAGH, NAAA, CLEC10A, LXN, and MCP-1, TRAIL, G-CSF, NBL1, and CCL23 as best discriminating proteins when comparing the long COVID group to groups of either healthy or COVID-19 recovered. Notably, longitudinal analysis indicated differences in the levels of a subset of plasma proteins following primary infection compared to after COVID-19 booster vaccination and breakthrough infection within the groups.</p> Conclusions: <p>These findings suggest that there is an altered immune response outcome primarily observed in individuals with long COVID upon re-exposure.</p>

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Divergent inflammatory and neurology-related protein levels in long COVID following primary and breakthrough SARS-CoV-2 infections

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月13日

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  • Amit Bansal,
  • Sam W. Z. Olechnowicz,
  • Nicholas Kiernan-Walker,
  • Jacob Cumming,
  • Imadh Abdul Azeez,
  • Ramin Mazhari,
  • Siavash Foroughi,
  • Jason A. Tye-Din,
  • Anna K. Coussens,
  • Vanessa L. Bryant,
  • Emily M. Eriksson,
  • Anne Hart,
  • Maureen Forde,
  • Nicholas Kiernan-Walker,
  • Ramin Mazhari,
  • Erin C. Lucas,
  • Mai Margetts,
  • Anthony Farchione,
  • Dylan Sheerin,
  • George Ashdown,
  • Rachel Evans,
  • Catherine Chen,
  • Shazia Ruybal-Pesántez,
  • Eamon Conway,
  • Marilou H. Barrios,
  • Jasper Cornish,
  • Maria Edmonds,
  • Lee M. Henneken,
  • Lisa J. Ioannidis,
  • Sam W. Z. Olechnowicz,
  • Ryan B. Munnings,
  • Joanna R. Groom,
  • Diana S. Hansen,
  • Rory Bowden,
  • Ivo Mueller,
  • Rebecca J. Cox,
  • Ivo Mueller,
  • Rory Bowden,
  • Emily M. Eriksson

摘要

Background:

Long COVID is a complex condition where symptoms persist for more than 3 months after SARS-CoV-2 infection and affects an estimated 5-30% of individuals. While persistent inflammation has emerged as an important feature of this condition, it is unclear if immune responses from COVID-19 vaccination or SARS-CoV-2 re-infection exacerbate or mirror the initial inflammatory responses.

Methods:

We quantified 182 inflammatory and neurology-related proteins in plasma using multiplexed affinity proteomics. Plasma samples from the COVID PROFILE cohort conducted in Victoria, Australia, were collected 6-9 months after first infection, but before COVID-19 vaccination from individuals who had recovered from COVID-19 (n = 21) or from individuals with long COVID (n = 12). To establish baseline plasma profiles, protein levels were benchmarked against unvaccinated, SARS-CoV-2 naive individuals (n = 24). In addition, we performed longitudinal analysis in a subset of individuals (n = 34), where paired samples collected 2-4 weeks after a third COVID-19 vaccine dose and after SARS-CoV-2 breakthrough infection were available to assess inflammatory and neurology protein plasma levels after antigen exposure in these contexts.

Results:

In this cohort Boruta feature selection and lasso regression models identified IL-20, HAGH, NAAA, CLEC10A, LXN, and MCP-1, TRAIL, G-CSF, NBL1, and CCL23 as best discriminating proteins when comparing the long COVID group to groups of either healthy or COVID-19 recovered. Notably, longitudinal analysis indicated differences in the levels of a subset of plasma proteins following primary infection compared to after COVID-19 booster vaccination and breakthrough infection within the groups.

Conclusions:

These findings suggest that there is an altered immune response outcome primarily observed in individuals with long COVID upon re-exposure.