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Human parainfluenza virus type 4 is incapable of evading the interferon-induced antiviral effect

Machiko Nishio1, Masato Tsurudome, Morihiro Ito

  • 1Department of Microbiology, Mie University School of Medicine, 2-174, Edobashi, Tsu-shi, Mie Prefecture, 514-8507 Japan. nishio@doc.medic.mie-u.ac.jp

Journal of Virology
|November 12, 2005
PubMed

Insights

Human parainfluenza virus type 4 V protein cannot evade interferon responses, unlike other paramyxoviruses. This inability is due to specific regions within its P/V common and V-specific domains.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Paramyxoviruses employ V proteins to counteract host interferon (IFN) responses by inactivating STAT proteins.
  • Human parainfluenza virus type 4 (hPIV4), a rubulavirus, possesses a V protein with a conserved cysteine-rich domain characteristic of paramyxovirus V proteins.

Purpose of the Study:

  • To investigate the function of the hPIV4 V protein in evading interferon-induced antiviral responses.
  • To determine if hPIV4 V protein can antagonize IFN signaling pathways.

Main Methods:

  • Established HeLa cells expressing the hPIV4A V protein (HeLa/FlagPIV4V).
  • Created chimeric V proteins between hPIV2 and hPIV4A V proteins.
  • Established HeLa cells persistently infected with hPIV4.
  • Analyzed STAT protein levels, tyrosine phosphorylation, and nuclear accumulation in response to IFN.

Main Results:

  • hPIV4 V protein did not reduce STAT1 or STAT2 levels but associated with STAT1, STAT2, DDB1, and Cul4A.
  • hPIV4 V protein did not interfere with STAT phosphorylation or IFN-induced STAT nuclear accumulation.
  • HeLa/FlagPIV4V cells remained sensitive to IFN-beta and IFN-gamma, indicating no blockage of IFN signaling.
  • The lack of IFN antagonism was attributed to both P/V common and V-specific domains, with specific regions identified (aa 32-45, 143-164, and 200-212).
  • hPIV4 was confirmed as the only analyzed paramyxovirus unable to evade IFN-induced antiviral responses.

Conclusions:

  • The hPIV4 V protein lacks the ability to antagonize interferon-induced antiviral responses.
  • Specific amino acid regions within the hPIV4 V protein are responsible for its inability to evade IFN signaling.
  • hPIV4 represents a unique paramyxovirus in its failure to escape host interferon defenses.

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