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A persistent variant of influenza C virus fails to interact with actin filaments during viral assembly

A Hechtfischer1, H Meier-Ewert, M Marschall

  • 1Abteilung für Virologie, Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, Germany.

Virus Research
|September 4, 1999
PubMed

Insights

Persistent influenza C virus variants alter viral assembly by changing nucleoprotein (NP) interactions with actin. This impacts progeny production and viral structure, unlike wild-type influenza viruses.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Influenza C virus infections can be persistent, characterized by reduced progeny production.
  • Viral assembly involves interactions between viral proteins like nucleoprotein (NP) and matrix (M) protein.
  • Cellular actin filaments play a role in the assembly of some viruses.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying persistent influenza C virus infections.
  • To compare the assembly characteristics of persistent influenza C variants with wild-type strains.
  • To elucidate the role of nucleoprotein (NP), matrix (M) protein, and actin in viral persistence.

Main Methods:

  • Infection of Madin-Darby canine kidney (MDCK) and Vero cells with influenza C/AA-pi virus and wild-type strains.
  • Immunofluorescence microscopy to visualize the distribution of NP and M proteins.
  • In vitro binding assays to assess NP-M protein interactions.
  • Cytochalasin D treatment to study the association of NP with actin filaments.

Main Results:

  • Persistent C/AA-pi virus showed homogeneous NP and M protein distribution, unlike the granular structures in wild-type infections.
  • NP and M proteins from wild-type and persistent viruses exhibited similar in vitro binding.
  • Wild-type NP associated with actin filaments, while persistent NP did not; this interaction was modulated by NP type.
  • Vero cells supported wild-type-like complex formation but not viral persistence.

Conclusions:

  • The interaction between NP, M protein, and actin is crucial for viral assembly.
  • Nucleoprotein (NP) plays a dominant role in modulating these interactions.
  • Altered NP-actin interaction is a key feature distinguishing persistent influenza C virus infection from wild-type strains.

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