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Paramyxovirus tropism dependent on host proteases activating the viral fusion glycoprotein

Y Nagai1, N M Inocencio, B Gotoh

  • 1Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Japan.

Behring Institute Mitteilungen
|July 1, 1991
PubMed

Insights

Paramyxovirus fusion glycoprotein cleavage dictates viral tropism. Researchers identified clotting factor Xa as a protease specific for monobasic cleavage sites, controlling localized infections.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Paramyxovirus fusion (F) glycoprotein requires posttranslational cleavage by host proteases for activation.
  • Cleavage site motif (monobasic vs. multibasic) influences protease specificity and viral tropism.
  • Ubiquitous proteases cleave multibasic sites, leading to pantropic infections.

Purpose of the Study:

  • To identify the host protease responsible for cleaving monobasic paramyxovirus F precursor glycoproteins.
  • To investigate the role of this protease in determining viral tropism.
  • To characterize proteases that cleave multibasic sites.

Main Methods:

  • Isolation and identification of chick embryo endoprotease specific for monobasic cleavage motif.
  • Ectopic expression of identified protease to assess its effect on viral tropism.
  • Induction of multibasic cleavage site processing using yeast KEX2 protease.

Main Results:

  • Identified chick embryo endoprotease as clotting factor Xa (FXa).
  • Ectopic expression of FXa determined viral tropism in chick embryos.
  • Yeast KEX2 protease, a subtilisin-like serine protease, induced cleavage at paired basic sites.

Conclusions:

  • Clotting factor Xa is a key determinant of paramyxovirus tropism through specific cleavage of monobasic F precursor sites.
  • Understanding protease specificity is crucial for controlling viral spread and pathogenesis.
  • Yeast KEX2 protease serves as a model for studying multibasic cleavage events.

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