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Glycoproteins M and N of human herpesvirus 8 form a complex and inhibit cell fusion

Shin Koyano1, Eng-Chun Mar1, Felicia R Stamey1

  • 1Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention, Mailstop G18, Herpesvirus Section, 1600 Clifton Road, Atlanta, GA 30333, USA.

The Journal of General Virology
|May 29, 2003
PubMed

Insights

Human herpesvirus 8 glycoproteins M and N (gM8/gN8) were analyzed. These viral proteins are essential for processing and form complexes, with gN8 required for gM8 function and conserved fusion inhibition.

Area of Science:

  • Virology
  • Molecular Biology
  • Glycoprotein Function

Background:

  • Herpesvirus glycoproteins M (gM) and N (gN) are conserved across the family.
  • Their roles in virus penetration and egress are established, particularly in alphaherpesviruses.
  • No prior studies investigated human herpesvirus 8 (HHV-8) gM (gM8) and gN (gN8) homologues.

Purpose of the Study:

  • To analyze the biochemical and functional characteristics of HHV-8 glycoproteins M (gM8) and N (gN8).
  • To determine the interaction and processing requirements between gM8 and gN8.
  • To investigate the potential conserved function of fusion inhibition in gammaherpesviruses.

Main Methods:

  • Biochemical analysis of gM8, including heat treatment aggregation and virion component identification.
  • Assessment of N-glycosylation for both gM8 and gN8.
  • Co-expression studies to analyze gM8/gN8 complex formation, processing dependency, and cell fusion inhibition.

Main Results:

  • gM8 exhibited heat-induced aggregation and was identified as a virion component.
  • Both gM8 and gN8 were found to be N-glycosylated.
  • gM8 formed a specific complex with gN8, and gN8 was essential for gM8's functional processing. Co-expression inhibited cell fusion induced by other viral proteins.

Conclusions:

  • HHV-8 gM8 and gN8 share biochemical properties with their alphaherpesvirus counterparts.
  • gN8 plays a crucial role in the functional processing of gM8.
  • Fusion inhibition, previously noted only in alphaherpesviruses, is a conserved function within the gammaherpesvirus subfamily, mediated by gM8 and gN8.

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