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(Theme 3) Tissue-specific and interferon-inducible expression of nonfunctional ACE2 through endogenous retrovirus co-option

  • Funded by UK Research and Innovation (UKRI)
  • Total publications:0 publications

Grant number: C19-IUC-359

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Key facts

  • Disease

    COVID-19

  • Start & end year

    N/A

  • Funder

    UK Research and Innovation (UKRI)

  • Principal Investigator

    George Kassiotis

  • Research Location

    United Kingdom

  • Lead Research Institution

    Francis Crick Institute

  • 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

    Not Applicable

  • Vulnerable Population

    Not applicable

  • Occupations of Interest

    Not applicable

Abstract

Angiotensin-converting enzyme 2 (ACE2) a human cell receptor targeted by the SARS-CoV-2 virus for entry into the cell. ACE2 has recently been proposed to be iduced by interferon and that SARS-CoV-2 may exploit this phenomenon to enhance viral spread. Crick researchers have identified a newly discovered isoform variant of ACE2 which is highly responsive to interferon stimulation, in stark contrast to canonical ACE2, also appears unstable and unable to bind SARS-CoV-2. The differences in physiology between these isoforms has implications for both interferon treatments of COVID-19 and virus transmission.