Decision support for prediction and management of Long Covid Syndrome (LCS)

Grant number: 101057553

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Key facts

  • Disease

    COVID-19
  • Start & end year

    2022
    2026
  • Known Financial Commitments (USD)

    $7,008,151.18
  • Funder

    European Commission
  • Principal Investigator

    Liira Helena
  • Research Location

    Finland
  • Lead Research Institution

    HUS-YHTYMA
  • Research Priority Alignment

    N/A
  • Research Category

    Clinical characterisation and management

  • Research Subcategory

    Prognostic factors for disease severity

  • Special Interest Tags

    N/A

  • Study Type

    Clinical

  • Clinical Trial Details

    Not applicable

  • Broad Policy Alignment

    Pending

  • Age Group

    Unspecified

  • Vulnerable Population

    Unspecified

  • Occupations of Interest

    Physicians

Abstract

We will develop tools and knowledge to support physicians in accurately managing Long COVID syndrome (LCS) which has a significant impact on sufferers as well as their surroundings. Although much is now known regarding appropriate clinical management of acute COVID-19, very little is known about clinical manifestations, risk factors and underlying mechanisms for development of the highly heterogenous LCS. In this project, we aim to understand and mechanisms of LCS by combining front-line expertise from the fields of clinical medicine, virology, metabolism and immunology. We will study the pathogenesis of LCS by conducting geographically diverse cohort and registry studies, by conducting mechanistic studies, by using novel high-throughput methods for biomarker analysis, and by conducting interventional and follow-up studies on LCS patients. We will combine results from clinical and mechanistic studies to identify molecular and physiological parameters and/or pathways to decipher the mechanisms underlying LCS. We will exploit the high-throughput omics technologies to identify the predisposing factors and biomarkers that lead to the development of LCS. We will collect data from the cohort, mechanistic, biomarker and interventional studies and use these to validate the predictive artificial intelligence algorithms and to produce information and gain understanding on the combination of factors that lead to certain clustering of patients into different groups with specific symptoms. A machine learning and AI-informed Long Covid Prediction Support (LCPS) tool will be developed for the use of clinicians to predict the LCS and its possible clinical manifestations in patients. It will also help in the choice of personalized treatments for LCS patients. Additionally, an interactive graphic user interface infographic will also be available to clinicians and patients; this will communicate novel and understandable information about LCS and recommendations for patient management.

Publicationslinked via Europe PMC

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Optimized summary-statistic-based single-cell eQTL meta-analysis.

Dynamin independent endocytosis is an alternative cell entry mechanism for multiple animal viruses.

Functioning of post-COVID-19 patients: a cross-sectional study at the outpatient clinic for long-term effects.

Ronapreve (REGN-CoV; casirivimab and imdevimab) reduces the viral burden and alters the pulmonary response to the SARS-CoV-2 Delta variant (B.1.617.2) in K18-hACE2 mice using an experimental design reflective of a treatment use case.

Sequential Infection with Influenza A Virus Followed by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Leads to More Severe Disease and Encephalitis in a Mouse Model of COVID-19.

Prognosis of patients with long COVID symptoms: a protocol for a longitudinal cohort study at a primary care referred outpatient clinic in Helsinki, Finland.

Symptom profiles and their risk factors in patients with post-COVID-19 condition: a Dutch longitudinal cohort study.

The Stereotypic Response of the Pulmonary Vasculature to Respiratory Viral Infections: Findings in Mouse Models of SARS-CoV-2, Influenza A and Gammaherpesvirus Infections.

SARS-CoV-2 Infection of Human Neurons Is TMPRSS2 Independent, Requires Endosomal Cell Entry, and Can Be Blocked by Inhibitors of Host Phosphoinositol-5 Kinase.