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Role of SUMOylation in Human Oncogenic Herpesvirus Infection

Yulin Zhang1, Yuyan Wang1, Caixia Zhu1

  • 1MOE& NHC&CAMS Key Laboratory of Medical Molecular Virology, Department of Medical Microbiology and Parasitology, School of Basic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China.

Virus Research
|April 14, 2020
PubMed

Insights

Small Ubiquitin-like Modifier (SUMO)ylation regulates key cellular processes and is exploited by oncogenic herpesviruses like Epstein-Barr Virus (EBV) and Kaposi's sarcoma-associated Herpesvirus (KSHV). This review details how these viruses manipulate SUMO pathways for replication and cancer development.

Area of Science:

  • Molecular Biology
  • Virology
  • Oncology

Background:

  • Post-translational modification by Small Ubiquitin-like Modifier (SUMO) is crucial for cellular functions like transcription, DNA repair, and chromosome segregation.
  • Oncogenic human herpesviruses, Epstein-Barr Virus (EBV) and Kaposi's sarcoma-associated Herpesvirus (KSHV), are linked to numerous human cancers.
  • The interaction between tumor viruses and SUMOylation has been a focus of recent research.

Purpose of the Study:

  • To review the current understanding of how SUMOylation influences the latent and lytic replication of EBV and KSHV.
  • To elucidate the mechanisms by which EBV and KSHV hijack SUMO pathways.
  • To highlight the role of these viral strategies in promoting host cell survival, proliferation, and virion production, contributing to cancer development.

Main Methods:

  • Literature review of studies investigating SUMOylation in EBV and KSHV infection.
  • Analysis of research on viral manipulation of host SUMO pathways.
  • Synthesis of findings related to SUMOylation's role in viral latency and lytic replication.

Main Results:

  • SUMOylation regulates both latent and lytic replication cycles of EBV and KSHV.
  • These oncogenic viruses employ sophisticated strategies to usurp host SUMO pathways.
  • Viral hijacking of SUMOylation promotes a cellular microenvironment conducive to host cell survival and proliferation during latency.
  • SUMOylation modulation is critical for reactivating virion production during the lytic phase.

Conclusions:

  • SUMOylation is a key regulatory mechanism exploited by EBV and KSHV.
  • Understanding the interplay between SUMOylation and these viruses is vital for comprehending EBV/KSHV-associated malignancies.
  • Targeting viral manipulation of SUMO pathways may offer therapeutic strategies against these cancers.

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