Abstract
Rabies virus infection is an endemic disease which remains central to public health issues. The presence of epigenetics associated with the over-expression of B7-H1 in mice brain infected with rabies virus was investigated for the first time. A significant increase (p < 0.05) in mRNA level of B7-H1 as the disease progressed was observed. The percentage of methylated region was significantly (p < 0.05) higher in infected tissues relative to uninfected. DNA methyltransferase (DNMT) and histone acetylase (HAT) activities were also significantly (p < 0.05) higher in most infected brain tissues. HAT had a relatively higher proportion than DNMT when compared to the normal. Paradoxically, it can be inferred that the rabies virus uses epigenetic mechanisms as a means of manipulating host genes, as there was an increase in global DNMT and HAT activities with concomitant increase in B7-H1 promoter methylation and expression.