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Mutations within the human parainfluenza virus type 3 (HPIV 3) C protein affect viral replication and host interferon

Greg Wells1, Matthew Addington-Hall, Achut G Malur

  • 1Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC 27834, USA.

Virus Research
|May 29, 2012
PubMed

Insights

Mutations in the human parainfluenza virus type 3 (HPIV-3) C protein impact viral replication and the host interferon response. Specific mutations differentially affect viral growth and the induction of interferon-beta (IFN-β).

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Human parainfluenza virus type 3 (HPIV-3) C protein inhibits viral replication and host interferon (IFN) signaling.
  • Phosphorylation sites on the HPIV-3 C protein influence its inhibitory activity.
  • Previous studies showed differential in vitro activities of C protein phosphorylation site mutants.

Purpose of the Study:

  • To generate and characterize HPIV-3 mutant viruses with specific C protein mutations.
  • To investigate the effect of C protein mutations on viral replication and host IFN induction.
  • To assess the ability of mutant viruses to overcome interferon-induced antiviral states.

Main Methods:

  • Generation of HPIV-3 mutant viruses (Cm-1, Cm-3, Cm-4) with mutations at S7, S47T48, and S81 residues of the C protein.
  • Analysis of viral replication profiles and transcription.
  • Assessment of IFN regulatory transcription factor 3 (IRF-3) activation and IFN-β mRNA levels using immunofluorescence and RT-PCR.
  • Evaluation of resistance to interferon-induced antiviral state in Vero cells.

Main Results:

  • All generated mutant viruses exhibited similar viral transcription.
  • The Cm-3 mutant showed relatively higher viral replication.
  • Infection with Cm-1 and Cm-3 induced IRF-3 activation and increased IFN-β mRNA.
  • Cm-3 demonstrated partial resistance to interferon-induced antiviral effects.

Conclusions:

  • Mutations within the HPIV-3 C protein differentially modulate viral replication.
  • Specific C protein mutations affect the induction of host interferon responses.
  • The study highlights the complex role of C protein phosphorylation sites in HPIV-3 pathogenesis.

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