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Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy
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Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

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Glycoprotein M is important for the efficient incorporation of glycoprotein H-L into herpes simplex virus type 1

Yudan Ren1, Susanne Bell1, Helen L Zenner1

  • 1Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.

The Journal of General Virology
|October 21, 2011
PubMed

Insights

Herpes simplex virus type 1 glycoprotein M (gM) is crucial for internalizing glycoprotein H-L (gH-L) during secondary envelopment. Its absence impairs viral entry and spread, highlighting gM's essential role in herpesvirus infection.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Herpes simplex virus type 1 glycoprotein M (gM) is a conserved type III membrane protein in Herpesviridae.
  • gM is generally considered non-essential, but its precise function in viral processes remains unclear.
  • Previous studies suggested gM's involvement in secondary envelopment and protein localization.

Purpose of the Study:

  • To investigate the role of gM in the localization and incorporation of viral envelope proteins during herpesvirus infection.
  • To analyze the impact of gM deletion on glycoprotein H-L (gH-L) internalization and virion assembly.
  • To determine the functional significance of gM in viral entry and cell-to-cell spread.

Main Methods:

  • Analysis of viral envelope protein localization and virion incorporation in cells infected with a gM-deletion virus and its revertant.
  • Utilizing transfection-based assays to study gM's ability to mediate protein internalization and targeting.
  • Assessing gH-L internalization from infected cell surfaces and its presence in assembled virions.

Main Results:

  • Absence of gM significantly inhibited the internalization of glycoprotein H-L (gH-L) from infected cell surfaces.
  • gM deletion did not affect the expression levels of gH and gL.
  • Virions produced without gM showed substantially reduced levels of gH-L, correlating with impaired viral entry and spread.

Conclusions:

  • gM plays a critical role in the specific internalization of gH-L.
  • gM is essential for the efficient targeting of gH-L to sites of secondary envelopment.
  • These findings reveal a key function for gM in herpesvirus replication and pathogenesis.

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