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Fusogenic variants of a noncytopathic paramyxovirus

Shaguna Seth1, Ioanna Skountzou, Kim M Gernert

  • 1Department of Microbiology and Immunology, Emory University School of Medicine, 1510 Clifton Road, Atlanta, GA 30322, USA.

Journal of Virology
|February 9, 2007
PubMed

Insights

Mutant strains of Sendai virus (SeV) were engineered to be fusogenic, unlike the wild-type virus. These mutants exhibited enhanced fusion and plaque formation, with specific genetic mutations identified in their F, HN, and M proteins.

Area of Science:

  • Virology
  • Molecular Biology
  • Structural Biology

Background:

  • Sendai virus (SeV) is a type 5 parainfluenza virus.
  • Wild-type SeV typically does not form syncytia (cell fusion).
  • This lack of fusion is linked to the cytoplasmic tail (CT) of the SeV F protein.

Purpose of the Study:

  • To investigate the genetic basis of SeV fusogenicity.
  • To identify mutations conferring syncytium-forming ability to SeV.
  • To understand the role of the F protein CT in viral fusion.

Main Methods:

  • Repeated passage of SeV to select for fusogenic mutants.
  • Viral replication assays.
  • Plaque assays to assess fusogenicity and plaque size.
  • Cloning and sequencing of viral genes (F, HN, M).
  • Structural analysis of the F protein.

Main Results:

  • Fusogenic SeV mutants were successfully generated.
  • Mutant viruses replicated comparably to or better than wild-type SeV.
  • Mutants formed plaques, unlike wild-type SeV, with varying plaque sizes.
  • Identified mutations in F protein (e.g., P22L, I191L), HN protein, and M protein (T129I).
  • Structural analysis pinpointed residues involved in mutant phenotypes.

Conclusions:

  • Specific mutations in SeV F, HN, and M proteins can confer fusogenic properties.
  • The F protein's cytoplasmic tail plays a role in regulating fusion.
  • Engineered fusogenic SeV mutants offer a model for studying paramyxovirus fusion mechanisms.

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