Infectious Pancreatic Necrosis Virus (IPNV) is one of the most prevalent viral pathogens affecting both wild and farmed salmonids worldwide. The disease caused by IPNV leads to high mortalities during the juvenile phase in the salmon industry.
Various studies have demonstrated that IPNV effectively evades the host’s antiviral responses.
A collaboration of researchers from the Universidad Austral de Chile (UACh), Universidad Andrés Bello (UNAB), the Interdisciplinary Center for Aquaculture Research (INCAR), and the Animal Health Research Center (CISA) in Spain has determined that Infectious Pancreatic Necrosis Virus (IPNV) can alter the expression of key genes in the rainbow trout immune system through epigenetic mechanisms.
Effect of Epigenetic Reprogramming
The study titled “Epigenetic reprogramming around IFN1 and IFNy2 promoters in rainbow trout cells inoculated with infectious pancreatic necrosis virus (IPNV),” authored by René Manríquez, Moisés Sandoval, Carlos Loncoman, Carolina Tafalla, Ruben Avendaño-Herrera, and Juan Guillermo Cárcamo, appears to be the first to demonstrate the effect of epigenetic reprogramming after IPNV infection in salmonid cells. “This demonstrates that the level of methylation/demethylation of the promoter and changes in the histone code associated with the promoters may play a role in modulating the immune response induced by the virus,” explain the researchers.
To achieve this, the researchers carried out an in silico characterization of the IFN1 and IFN2 promoters in rainbow trout, identifying CpG dinucleotide-rich regions (islands) and putative transcription factor binding sites (TBS) for both gene promoters. Subsequently, they infected RTS11 cells (rainbow trout monocytes/macrophages) with IPNV and monitored the course of viral infection for 48 hours.
In broad terms, the experts found that IPNV-infected cells showed increased transcriptional expression of IFN1 and IFN2 at 6 and 24 hours post-infection, respectively. The infection also caused increases and decreases in the global methylation of the IFN2 promoter at 6 and 24 hpi, respectively. On the other hand, the IFN1 promoter remained completely unmethylated throughout the infection course, similar to the control.
Conclusion
“These results suggest that IPNV epigenetically modulates the expression of IFN1 by altering the levels of acetylation of the H4 histones associated with its promoter. Additionally, the modulation of IFN2 expression would be through changes in the levels of methylation/demethylation of its promoter, along with changes in the levels of acetylation of the H4 histones associated with this promoter,” they concluded.
The study was funded by the National Fund for Scientific and Technological Development of Chile (FONDECYT), the Fund for the Promotion of Scientific and Technological Development (FONDEF), and the Fund for the Financing of Research Centers in Priority Areas (FONDAP).
Reference
René A. Manríquez, Moisés Sandoval, Carlos Loncoman, Carolina Tafalla, R. Avendaño-Herrera, Juan G. Cárcamo. 2023. Epigenetic reprogramming around IFN1 and IFNy2 promoters in rainbow trout cells inoculated with infectious pancreatic necrosis virus (IPNV), Fish & Shellfish Immunology, Volume 140, 2023, 108947, ISSN 1050-4648, https://doi.org/10.1016/j.fsi.2023.108947.
