ARS | Publication request: Characterization of Chicken Stem Cell Antigen 2 and Initial Investigation of Its Role in Marek's Disease Virus Infection

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: July 25, 2009
Publication Date: July 25, 2009
Citation: Mao, W., Hunt, H.D., Kim, T., Cheng, H.H. 2009. Characterization of Chicken Stem Cell Antigen 2 and Initial Investigation of Its Role in Marek's Disease Virus Infection [abstract]. 34th International Herpesvirus Workshop, Ithaca, New York, July 25-30, 2009. Paper No. 2.15.

Technical Abstract: Chicken stem cell antigen 2 (SCA2) has been proposed as a Marek’s disease (MD) resistant gene due to the following criteria: (1) genetic association to MD resistance, (2) transcriptional differences between MD resistant and susceptible experimental chicken lines following challenge with Marek’s disease virus (MDV), and (3) direct protein interaction with MDV US10 as determined by a two-hybrid screen followed by an in vitro binding assay. The majority of work characterizing SCA2 has been done in mouse. In mouse, SCA2 is a member of lymphostromal cell membrane Ly-6 superfamily, which regulates the intracellular signaling via T cell receptor and cell-cell adhesion as a receptor on the lymphocyte membrane. To investigate the biochemical properties of chicken SCA2 and its role in MDV infection, chicken SCA2 was expressed and purified in E. coli, and a polyclonal antibody developed. Utilizing the anti-SCA2 polyclonal antibody, SCA2 is a 13 kD cell surface protein anchored by a glycosyl-phosphatidylinositol (GPI) moiety. SCA2 was detected on the cell surface of a reticuloendotheliosis (REV) transformed avian T lymphoid cell line but not on the surface of T and B cells collected from thymus, spleen and bursa in 4-week old birds. SCA2 was expressed in liver cells and connective cells of thymus and bursa based on immunohistochemistry, immunoprecipitation and western blots. In bursa follicles, SCA2 is specifically expressed on the cortical-medullary epithelial cells surrounded by MHC class II presenting cells, which suggest that SCA2 may play role in B cell development by interacting with ligands displayed on the B cell surface. With respect to MDV infection, SCA2 up-regulation was detected both in RP-1 avian T lymphoid cells induced for MDV replication and in the bursa of MDV-challenged birds. SCA2 and MDV US10 also co-localize in DF1-SCA2Flag cells infected with MDV. These data suggests SCA2 may play role in MDV lytic infection and MDV US10 may be involved into this process.