The use of replication-competent hepatitis B virus (HBV) DNA to construct a mouse model will help explore antiviral treatment strategies for more than 240 million patients infected with HBV worldwide. Eradication of chronic HBV infection can effectively block the adverse consequences of HBV-induced hepatic cirrhosis, failure and carcinoma. The core reason that HBV is difficult to eradicate is that most of infected people develop chronic HBV infection due to the establishment of immune tolerance. Here, we introduce a mouse model of adeno-associated virus (AAV)-HBV transfection, which produces HBV surface antigen (HBsAg) that can be maintained for more than 6 months. During virus replication, intermediates, transcripts, and proteins can be detected in peripheral blood. At the same time, the prerequisite for studying liver disease formation and immunotherapy through in vitro experiments is to isolate hepatic subgroup cells. Here, we describe a cell sorting method based on liberase perfusion technology combined with low-speed centrifugation and magnetic bead antibody labeling to purify hepatic parenchymal cells (PCs) and non-parenchymal cells (NPCs) step by step from murine liver, such as hepatic sinusoidal endothelial cells (LSECs) and Kupffer cells (KCs), which will help accelerate the study of the genetic and clearance mechanistic of chronic HBV infection.
Part of the book: Hepatitis B
Human cytomegalovirus (HCMV) retinitis accounts for 70% of herpesvirus-infected ocular diseases. Recent advances in knowledge of innate immune responses to viral infections have elucidated a complex network of the interplay between the invading virus, the target cells, and the host immune responses. Ocular cytomegalovirus latency exacerbates the development of choroidal neovascularization. Viruses have various strategies to evade or delay the cytokine response, and buy time to replicate in the host. Some signaling proteins impact the virologic, immunologic, and pathological processes of herpesvirus infection with particular emphasis on retinitis caused by HCMV. The accumulated data suggest that signaling proteins can differentially affect the severity of viral diseases in a highly cell-type-specific manner, reflecting the diversity and complexity of herpesvirus infection and the ocular compartment. By summarizing the immunological characteristics and pathogenesis of HCMV ocular infection, it will provide important information on the development of antiviral therapy, immunotherapy, and antidrug resistance.
Part of the book: Viral Outbreaks