Suppression of human metapneumovirus (HMPV) infection by the innate sensing gene CEACAM1

Mohammad Diab1, Alon Vitenshtein1, Yaron Drori2,3

  • 1The Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel Canada of the Faculty of Medicine, The Hebrew University Hadassah Medical School, Jerusalem, Israel.

Oncotarget
|September 17, 2016
PubMed

Insights

Human Metapneumovirus (HMPV) infection triggers the RIG-I sensor, upregulating CEACAM1. This protein then suppresses viral loads by inhibiting translation machinery, effectively restricting HMPV replication.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Innate immunity relies on pattern recognition receptors (PRRs) to detect pathogen-associated molecular patterns (PAMPs).
  • Human Metapneumovirus (HMPV) is a significant respiratory pathogen in children, necessitating understanding of host-virus interactions.

Purpose of the Study:

  • To investigate the innate immune response to HMPV infection.
  • To elucidate the role of CEACAM1 in HMPV pathogenesis.

Main Methods:

  • Detection of viral RNA using RIG-I sensor upon HMPV infection.
  • Analysis of CEACAM1 promoter activity and IRF3 binding.
  • Assessment of viral load and protein translation inhibition.

Main Results:

  • HMPV infection induces CEACAM1 expression via IRF3 binding to its promoter.
  • Induced CEACAM1 suppresses HMPV viral loads.
  • CEACAM1-mediated suppression occurs through SHP2-dependent inhibition of the translation machinery.

Conclusions:

  • HMPV-infected cells upregulate CEACAM1 as a mechanism to restrict viral infection.
  • This study reveals a novel antiviral pathway involving CEACAM1 and SHP2.

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