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The nucleocapsid protein of measles virus blocks host interferon response

Ikuyo Takayama1, Hiroki Sato, Akira Watanabe

  • 1Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.

Virology
|January 10, 2012
PubMed

Insights

Measles virus (MV) P/V/C proteins and notably the N protein antagonize host interferon (IFN) signaling. MV-N protein blocks STAT nuclear import, inhibiting the immune response.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Paramyxoviruses, including Measles virus (MV), employ diverse mechanisms to inhibit host interferon (IFN) signaling pathways.
  • Previous studies suggested P/V/C proteins of MV interfere with IFN pathways, but inconsistencies exist.

Purpose of the Study:

  • To confirm the effects of MV P gene products on IFN pathways.
  • To investigate the role of other MV proteins, particularly the N protein, in modulating host IFN responses.
  • To elucidate the mechanism by which MV-N protein inhibits IFN signaling.

Main Methods:

  • Analysis of MV P gene products' effects on IFN pathways.
  • Examination of other MV viral proteins' impact on IFN signaling.
  • Investigation into the mechanism of MV-N mediated inhibition, including STAT activation, degradation, and nuclear import.

Main Results:

  • MV P gene products were confirmed to affect IFN pathways.
  • MV N protein was identified as a potent antagonist of IFN-α/β and IFN-γ signaling, comparable to P gene products.
  • MV-N inhibits IFN signaling by blocking the nuclear import of activated STAT, without affecting STAT/Jak activation or degradation.
  • Nuclear translocation of MV-N is crucial for its inhibitory function.
  • The inhibitory role of the N protein was found to be conserved among other morbilliviruses.

Conclusions:

  • Both P/V/C proteins and the N protein of Measles virus are involved in suppressing host IFN signaling pathways.
  • The N protein's ability to block STAT nuclear import represents a significant mechanism for immune evasion by MV.
  • The findings highlight the N protein as a key viral factor in morbillivirus-host immune interactions.

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