New Research from the Frappier Lab: Breaking Down EBV's Defence
How EBV Fights Back: Protein Changes and Viral Tricks
Researchers from the Department of Molecular Genetics at the University of Toronto have revealed a cellular defence mechanism against the Epstein-Barr virus (EBV). The findings, recently published in the journal PLOS Pathogens, as "Changes in SUMO-modified proteins in Epstein-Barr virus infection identifies reciprocal regulation of TRIM24/28/33 complexes and the lytic switch BZLF1," highlight the virus's strategy to disable this defence, providing crucial insights into the molecular interactions that occur during EBV infection. Let's explore this new study and its significance in the fight against EBV.
Researchers at Frappier's Lab, led by Carlos F. De La Cruz-Herrera and Umama Z. Siddiqi, a current PhD student, conducted a study on SUMO-modified proteins in EBV infections. SUMO modification is a process that regulates protein function and is linked to the regulation of herpesvirus infections, including EBV. The researchers found changes in SUMO modification during EBV reactivation in the TRIM24/TRIM28/TRIM33 complex, which is crucial for antiviral responses.
The Trio of Protectors: This research highlights how the three proteins (TRIM24, TRIM28, and TRIM33) work together as essential components of the body's immune response to stop the Epstein-Barr virus (EBV) from replicating. These proteins use complex methods to inhibit EBV's lytic infection by suppressing the expression of the first lytic protein, BZLF1. By doing so, they prevent the creation of new viral particles, slowing down the spread of EBV in the body.
The Virus's Sneaky Countermeasure: Despite challenges, EBV is resilient and has developed a smart way to evade the body's immune system. During EBV reactivation, the virus produces BZLF1, which interacts with TRIM24 and TRIM33, disrupting their stability and functionality, rendering them powerless in their mission to combat the virus. This compromises the body's defence mechanisms, allowing EBV to continue replicating and evading the host's immune response.
Implications and Future Prospects: Though often causing no noticeable symptoms, the Epstein-Barr virus is a significant pathogen connected to various types of cancer and multiple sclerosis. Understanding the complex interaction between viral proteins and cellular defences is important in developing effective strategies to combat EBV-associated diseases.
"This paper provides new insights into how Epstein-Barr virus (EBV) manipulates cellular proteins to overcome antiviral restrictions and enable efficient virus production," remarked Lori Frappier, the Molecular Genetics Professor leading the research team. "This information provides new opportunities for disabling EBV protein functions to inhibit lytic infection, which would decrease the high viral load associated with EBV-induced cancers."
