Use of patient-relevant human lung epithelial cell models to study acute and long-term effects of COVID-19

  • Funded by Netherlands Organisation for Health Research and Development (ZonMW)
  • Total publications:2 publications

Grant number: 114025007

Grant search

Key facts

  • Disease

    COVID-19
  • Start & end year

    2020
    2022
  • Known Financial Commitments (USD)

    $548,404.84
  • Funder

    Netherlands Organisation for Health Research and Development (ZonMW)
  • Principal Investigator

    Dr. AM van der Does
  • Research Location

    Netherlands
  • Lead Research Institution

    Leiden University Medical Center
  • Research Priority Alignment

    N/A
  • Research Category

    Pathogen: natural history, transmission and diagnostics

  • Research Subcategory

    Pathogen morphology, shedding & natural history

  • Special Interest Tags

    N/A

  • Study Type

    Non-Clinical

  • Clinical Trial Details

    N/A

  • Broad Policy Alignment

    Pending

  • Age Group

    Unspecified

  • Vulnerable Population

    Unspecified

  • Occupations of Interest

    Unspecified

Abstract

Project description The lung epithelium lines the airways and alveoli, and is the main cell type infected by SARS-COV-2, the virus that causes COVID-19. Mapping and understanding the lung epithelial response to SARS-CoV-2 infection is needed to better understand the short and long-term effects of the infection and the severity of COVID-19. In this project, we use our non-animal culture models for this. We will investigate how the epithelium obtained from different locations (from nose to alveoli) responds to infection with SARS-CoV-2. It also compares the epithelium response to SARS-CoV-2 with that to other coronaviruses to investigate what makes this virus so special. Furthermore, epithelial cells and immune cells from COVID-19 patients are compared with those from healthy persons.

Publicationslinked via Europe PMC

SARS-CoV-2-infected human airway epithelial cell cultures uniquely lack interferon and immediate early gene responses caused by other coronaviruses.

Prolonged activation of nasal immune cell populations and development of tissue-resident SARS-CoV-2-specific CD8+ T cell responses following COVID-19.