CD4 encodes a glycoprotein, located on the surface of T helper (Th) cells and regulatory T cells. Through interaction with MHC class II molecules, CD4 directs the linage development of Th cells in immune organs and activates the CD4+ T cell maturation process . Thus, the transcriptional level of CD4 is directly related to T cell development . In mice, CD4 transcription is controlled by several cis-acting elements including enhancers, silencers and DNA methylation [3, 4]. However, the epigenetic regulation of CD4 gene in chicken and its relationship with any virus infection are still unclear.⋯
Marek’s disease (MD), a T cell lymphoma of chickens caused by the Marek’s disease virus (MDV), is characterized by mononuclear cell-infiltration in various organs including peripheral nerves, skin, muscle, and visceral organs , and is a worldwide problem for the poultry industry. A complex MDV life cycle was found in susceptible chickens during MD progression, which includes an early cytolytic phase (2-7 days post infection, dpi), latent phase (7-10 dpi), late cytolytic phase (from 18 dpi) and transformation phase (28 dpi and onwards) .
Epigenetics is the study of alterations that result in inherited changes in phenotypes despite the lack of DNA sequence polymorphisms and include DNA methylation, histone modification and chromatin remodeling . It is described as the interaction between genes and environmental factors. Aberrant CpG methylation levels of the gene promoter region contribute to oncogenesis . Viruses are one of the environmental agents that can cause alterations of DNA methylation level in host genes .
The focus of this study was to better understand the expression control of CD4 by ascertaining the epigenetic status in the CD4 promoter and the CD4 expression in relation to MDV infection. Two inbred chicken lines, MD-resistant or –susceptible with the same MHC (major histocompatibility complex) haplotypes, from Avian Disease and Oncology laboratory (ADOL) were used . We, therefore, measured the promoter methylation and transcription of the CD4 gene before and after MDV infection of both lines. We found methylation alterations in the CD4 promoter region after MDV infection differ between these two lines.