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Long COVID endotheliopathy: hypothesized mechanisms and potential therapeutic approaches

Jasimuddin Ahamed1, Jeffrey Laurence2

  • 1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.

The Journal of Clinical Investigation
|August 1, 2022
PubMed

Insights

Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), is a multi-organ disorder with unknown causes. Research suggests microvascular endotheliopathy and inflammation may drive PASC pathology.

Area of Science:

  • Infectious Diseases
  • Immunology
  • Pathophysiology

Background:

  • Long COVID (post-acute sequelae of SARS-CoV-2 infection, PASC) is a complex, multi-organ disorder following SARS-CoV-2 infection.
  • Current understanding of PASC pathophysiology, incidence, and effective treatments remains limited.
  • While acute COVID-19 involves systemic inflammation and macrovascular thrombosis, PASC exhibits distinct clinical and pathological features.

Purpose of the Study:

  • To explore the underlying pathophysiology of PASC, differentiating it from acute COVID-19.
  • To identify potential diagnostic markers and therapeutic targets for PASC.
  • To investigate factors influencing PASC risk, such as sex at birth.

Main Methods:

  • Review of clinical phenotypes and biomarker data in acute COVID-19 versus PASC.
  • Analysis of potential mechanisms including microvascular endotheliopathy, viral reservoirs, autoantibodies, and pathogen reactivation.
  • Examination of PASC tissue pathology, including microvascular thrombosis.

Main Results:

  • PASC is characterized by persistent microvascular endotheliopathy, potentially linked to SARS-CoV-2 tissue reservoirs.
  • Unlike acute COVID-19, macrovascular thrombosis is less frequent in PASC.
  • Female sex at birth is associated with lower acute COVID-19 risk but higher PASC risk.
  • Evidence suggests autoantibodies, localized inflammation, and pathogen reactivation may contribute to PASC, potentially causing microvascular thrombosis.

Conclusions:

  • Persistent microvascular endotheliopathy and localized inflammation are key suspected drivers of PASC.
  • Further research into diagnostic assays targeting these mechanisms could reveal therapeutic strategies for Long COVID.
  • Understanding PASC's distinct pathophysiology is crucial for developing effective treatments.

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