AI Article Synopsis

  • * They achieve this by interfering with the host's post-translational modification activities, using various proteins like kinases and ubiquitin ligases.
  • * The review specifically examines how three oncoviruses (EBV, KSHV, and HIV) interact with the ubiquitin-proteasome system through their own or host's E3 ubiquitin ligase functions.

Article Abstract

For productive infection and replication to occur, viruses must control cellular machinery and counteract restriction factors and antiviral proteins. Viruses can accomplish this, in part, via the regulation of cellular gene expression and post-transcriptional and post-translational control. Many viruses co-opt and counteract cellular processes via modulation of the host post-translational modification machinery and encoding or hijacking kinases, SUMO ligases, deubiquitinases, and ubiquitin ligases, in addition to other modifiers. In this review, we focus on three oncoviruses, Epstein-Barr virus (EBV), Kaposi's sarcoma herpesvirus (KSHV), and human immunodeficiency virus (HIV) and their interactions with the ubiquitin-proteasome system via viral-encoded or cellular E3 ubiquitin ligase activity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10535929PMC
http://dx.doi.org/10.3390/v15091935DOI Listing

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