The involvement of HBV infection in epigenetic alternations during hepatocarcinogenesis has been described; HBV X (HBx) protein expression promoted DNA methyltransferase (DNMT) activity by upregulation of DNMT1, DNMT3A1, and
DNMT3A2 and selectively facilitated regional hypermethylation of specific tumor suppressor genes [4].
Figure 2 shows the structure of DNMT3A; the human enzyme has two known splice isoforms DNMT3A1 and DNMT3A2 [50].
The main difference between the two splice isoforms of DNMT3A1 and DNMT3A2 is the extra DNA binding domain located at the amino terminal of DNMT3A1.
The virus contained extra copies of a gene that makes an enzyme called DNA methyltransferase (Dnmt3a2).
When the researchers used similar techniques to halve the amount of Dnmt3a2 that young mice produce, their performance deteriorated to that of non-treated elderly mice.