A second and more thoroughly characterized root cause of the pathology in CHD is traced to immunological effects such as: (i) excessive recruitment of inflammatory cells due to NFkb upregulation, resulting in the production of TNFα and other innate cytokines; (ii) inhibition of type 1 interferon (T1IFN) signaling, and; (iii) HDV-specific Th1 CD4- and CD8 cytotoxic T cell responses, which although likely beneficial for the ability to clear HDV infected cells cause tissue damage if proper immune regulation (e.g., PD-1) is absent or insufficient. Here, CD8A is linked to coronary artery disorder.