Related Experiment Video

Updated: Jun 1, 2026

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy
06:40

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

Published on: November 4, 2018

Host cell protein C9orf69 promotes viral proliferation via interaction with HSV-1 UL25 protein

Ying Zhang1, Yan-Mei Li, Long-Ding Liu

  • 1Institute of Medical Biology, Chinese Academy of Medicine Science & Peking Union Medical College, Kunming, China.

Virologica Sinica
|June 14, 2011
PubMed

Insights

Researchers identified C9orf69 as a novel host protein interacting with herpes simplex virus type 1 (HSV-1) UL25 protein. This interaction promotes viral proliferation, offering new insights into HSV-1 replication mechanisms.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • Herpes simplex virus type 1 (HSV-1) is a significant human pathogen.
  • The interaction between viral proteins and host cell factors is crucial for viral replication.
  • Limited information exists regarding the host proteins interacting with HSV-1 nucleocapsid protein UL25.

Purpose of the Study:

  • To identify host cell proteins that interact with the HSV-1 UL25 protein.
  • To investigate the functional role of identified interacting proteins in HSV-1 infection.

Main Methods:

  • Yeast two-hybrid screening was employed to identify UL25-interacting proteins.
  • Co-localization by fluorescence and immunoprecipitation assays were used to confirm interactions under physiological conditions.

Main Results:

  • The cellular protein C9orf69 was identified as an interactor of HSV-1 UL25.
  • The interaction between C9orf69 and UL25 was validated using co-localization and immunoprecipitation.
  • C9orf69 was found to promote viral proliferation.
  • C9orf69 promotes proliferation indirectly through its interaction with UL25, not by regulating viral gene transcription.

Conclusions:

  • C9orf69 is a novel host factor that interacts with HSV-1 UL25.
  • The UL25-C9orf69 interaction plays a role in enhancing HSV-1 proliferation.
  • This finding provides new targets for understanding and potentially controlling HSV-1 infection.

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