Host cellular signaling induced by influenza virus

Sci China Life Sci. 2011 Jan;54(1):68-74. doi: 10.1007/s11427-010-4116-z. Epub 2011 Jan 21.

Abstract

A wide range of host cellular signal transduction pathways can be stimulated by influenza virus infection. Some of these signal transduction pathways induce the host cell's innate immune response against influenza virus, while others are essential for efficient influenza virus replication. This review examines the cellular signaling induced by influenza virus infection in host cells, including host pattern recognition receptor (PRR)-related signaling, protein kinase C (PKC), Raf/MEK/ERK and phosphatidy-linositol-3-kinase (PI3K)/Akt signaling, and the corresponding effects on the host cell and/or virus, such as recognition of virus by the host cell, viral absorption and entry, viral ribonucleoprotein (vRNP) export, translation control of cellular and viral proteins, and virus-induced cell apoptosis. Research into influenza virus-induced cell signaling promotes a clearer understanding of influenza virus-host interactions and assists in the identification of novel antiviral targets and antiviral strategies.

MeSH terms

  • Eukaryotic Initiation Factor-4E / metabolism
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate / physiology
  • Influenza, Human / physiopathology
  • Orthomyxoviridae / metabolism*
  • Orthomyxoviridae / pathogenicity
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Kinase C / metabolism
  • Receptors, Retinoic Acid / metabolism
  • Signal Transduction / physiology*
  • Toll-Like Receptors / metabolism
  • Viral Proteins / genetics
  • Viral Proteins / metabolism
  • Virus Internalization

Substances

  • Eukaryotic Initiation Factor-4E
  • Receptors, Retinoic Acid
  • Toll-Like Receptors
  • Viral Proteins
  • Phosphatidylinositol 3-Kinases
  • Protein Kinase C