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Related Experiment Videos

SARS-coronavirus replication in human peripheral monocytes/macrophages.

Mamadi Yilla1, Brian H Harcourt, Carole J Hickman

  • 1Respiratory and Enteric Viruses Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Rd., MS-C22, Atlanta, GA 30333, USA. mby7@cdc.gov

Virus Research
|November 30, 2004
PubMed
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Severe acute respiratory syndrome coronavirus (SARS-CoV) poorly infects human monocytes/macrophages, similar to human coronavirus OC43. Interferon-alpha production by these immune cells further limits SARS-CoV replication, impacting disease course.

Area of Science:

  • Virology
  • Immunology
  • Infectious Diseases

Background:

  • A novel coronavirus, SARS-CoV, is associated with severe acute respiratory syndrome.
  • Human coronaviruses 229E and OC43 exhibit differential infectivity in human monocytes/macrophages.
  • Understanding SARS-CoV's interaction with immune cells is crucial for comprehending SARS pathogenesis.

Purpose of the Study:

  • To investigate the productive infection of purified human monocytes/macrophages (PM) by SARS-CoV.
  • To compare SARS-CoV infectivity in PM with that of human coronaviruses 229E and OC43.
  • To explore the role of interferon-alpha (IFN-alpha) in modulating SARS-CoV infection of PM.

Main Methods:

  • Infection of human donor-derived purified monocytes/macrophages (PM) with SARS-CoV, HCoV-229E, and HCoV-OC43.

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  • Quantification of viral titers (TCID50/ml) in infected cells.
  • Detection of SARS-CoV proteins within PM.
  • Assessment of IFN-alpha production by PM.
  • Preliminary electron microscopy to visualize viral entry.
  • Main Results:

    • SARS-CoV replicated poorly in PM, yielding low viral titers (10^1.75 to 10^2 TCID50/ml), comparable to OC43 (10^1.2 to 10^2.7 TCID50/ml).
    • Human coronavirus 229E showed higher replication in PM (10^3.5 to 10^6 TCID50/ml).
    • SARS-CoV proteins were detected primarily in PM with low IFN-alpha production; viral particles appeared to enter cells via phagocytosis.

    Conclusions:

    • SARS-CoV exhibits limited productive infection in human monocytes/macrophages, similar to HCoV-OC43.
    • IFN-alpha production by PM appears to restrict SARS-CoV replication.
    • The interaction between SARS-CoV, monocytes/macrophages, and IFN-alpha may significantly influence the clinical course of SARS.