Rabies virus infection in mice up-regulates B7-H1 via epigenetic modifications
- PDF / 418,569 Bytes
- 7 Pages / 595.276 x 790.866 pts Page_size
- 2 Downloads / 181 Views
SHORT COMMUNICATION
Rabies virus infection in mice up-regulates B7-H1 via epigenetic modifications Comfort E. Ojedapo1,3 • Aliyu Muhammad1,3 • Grace S. N. Kia2,3 • Musa M. Abarshi1,3 • Maryam Abdulazeez1,3 • Joy Cecilia Atawodi2 • Jacob K. P. Kwaga2,3
Received: 9 July 2019 / Accepted: 24 April 2020 Ó Indian Virological Society 2020
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 B7H1 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. Keywords Rabies virus infection B7-H1 Promoter region DNA methylation Histone acetylation
& Aliyu Muhammad [email protected] 1
Department of Biochemistry, Faculty of Life Sciences, Ahmadu Bello University, Zaria, Kaduna State, Nigeria
2
Department of Public Health and Preventive Medicine, Ahmadu Bello University, Zaria, Nigeria
3
Africa Centre of Excellence for Neglected Tropical Diseases and Forensic Biotechnology, Ahmadu Bello University Centre, Zaria, Nigeria
Rabies virus (RABV) causes about 55,000 human deaths globally each year and the vast majority of deaths (84%) occur in rural areas [25]. It is an endemic disease which remains an important public health issue in Nigeria and other African countries [18]. The rabies virus is a bullet shaped negative single stranded Ribonucleic Acid (RNA) virus and a member of the genus Lyssavirus in the Rabdoviridae family. It is neurotropic and causes fatal encephalitis in mammals [22]. The virus consists of 12 kb strand RNA genome which encodes for five different proteins [2]. The virus is usually transmitted by the saliva of an infected animal after bites or scratches [18]. It then enters the central nervous system (CNS) through retrograde transport and undergoes rapid viral replication from where it reaches the salivary glands and excreted in saliva, at this stage it can be transmitted to a new host [4]. Once the disease is established in the brain, it leads to nearly 100% mortality rate in humans if timely post-exposure prophylaxis is not administered [22]. The rabies virus (RABV) has developed an immuno-subversive strategy by up-regulating the expression of molecules such as B7-H1 [13]. B7 homolog 1 (B7-H1) also known as programmed death ligand-1(PD-L1) or CD274 is a B7 family member that inhibits T-cel
Data Loading...
