To methylate, or not to methylate? That is the question. Whether ’tis nobler in the genome to suffer the onslaughts and diversions of oncogenic DNA viruses or, by inactivating, disguise them (from immune surveillance).
When researchers used bisulfite sequencing to examine the methylomes of three double-stranded DNA viruses (Human Papilloma Viruses (HPV) 16 and 18, and Hepatitis B Virus (HBV)), and that of the transcription start sites of another (Epstein-Barr Virus, EBV), they found a curious thing. Free particles and viruses in otherwise healthy tissue were unmethylated. Yet the further along toward full-blown, invasive cancer the tissue was, the more methylated the virus sequences were. Thus, viral methylation may be a “mark” of disease progression.
Viruses can code for proteins (for example, HPV E2) that can keep cells from proliferating: prevent their expression and disease can ensue. And of course, by keeping expression down to a trickle, these transformed cells may be able to remain undetected. Follow the reasoning at Genome Research, February 2009