Open AccessRabies virus infection in mice up-regulates B7-H1 via epigenetic modifications
Author(s) -
Comfort E Ojedapo,
Aliyu Muhammad,
G.S.N. Kia,
M. M. Abarshi,
Maryam Abdulazeez,
Joy C. Atawodi,
Jacob K. P. Kwaga
Publication year - 2020
Publication title -
virusdisease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.375
H-Index - 22
eISSN - 2347-3517
pISSN - 2347-3584
DOI - 10.1007/s13337-020-00588-w
Subject(s) - epigenetics , rabies virus , rabies , biology , virology , virus , histone , dna methyltransferase , methyltransferase , dna methylation , methylation , gene , gene expression , genetics
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.