Viral infection has emerged as one of the leading causes of human cancers, accounting for 10-15% of human cancer worldwide. Infections can alter epigenetic patterns and lead to irregular growth of host cells that activate oncogenic pathways. Epigenetic variations are changes in chromatin rather than genomic ...
Viral infection has emerged as one of the leading causes of human cancers, accounting for 10-15% of human cancer worldwide. Infections can alter epigenetic patterns and lead to irregular growth of host cells that activate oncogenic pathways. Epigenetic variations are changes in chromatin rather than genomic sequence that can make transcriptional reprogramming and binding pattern remodeling of transcription factors. DNA methylation, histone modifications and some non-coding RNA (ncRNA) changes are the main ways of epigenetic changes, which evolved as means of regulating cell growth and differentiation, as well as providing molecular memory that leads to abnormal development. Host cells will undergo epigenetic changes upon viral stimuli to promote altered binding sites of transcription factors and transcriptional reprogramming as resistance. At the same time, epigenetic modifications can also enhance the function of the viral genome and bring the virus into a latent state where gene expression is suppressed. siRNA-mediated viral splicing has been demonstrated as a main anti-viral immune activity in plants. Meanwhile, it has been widely understood that Epstein-Barr virus (EBV) requires epigenetic changes in the viral genome to maintain productive amplification in the host. EBV also induces changes in host chromatin accessibility that facilitate viral latency and amplification, which in turn alter the transcription profile that is associated with hematologic malignancies. However, it is poorly understood which key transcription factors are involved in the recruitment of transcripts and by what types of modifications they regulate gene expression.
This Research Topic focuses on the mechanism of epigenetic changes upon viral infection, especially those that lead to other diseases in the host. Further research on the relationship between epigenetics and transcriptome of the infected host will open another door to anti-virus immunity, discovering a newer layer of host epigenetic regulation upon viral infection for the development of targeted therapies that alter the epigenetic changes and maximizing host immunity to suppress and clear the virus.
We welcome submissions of Original Research and Reviews, focusing on but not limited to the following subtopics:
• Transcriptional reprogramming caused by epigenetic changes in different hosts, including mammals and plants
• Chromatin conformation in viral infection
• The balance between chromatin remodeling and anti-inflammatory
• Key transcription factors that drive infection-caused disease
• Epigenetic changes in the viral community and their relation to tumor progression
• Epigenetically related therapeutic strategies for tumors caused by viral infections
Keywords:
epigenetics, chromatin remodeling, transcription, anti-inflammatory
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.