Despite active immune responses, dapoxetine establish latency. In a related process, these viruses also persistently replicate by using a mechanism that requires different viral genes than acute-phase replication. Many questions remain about the role of immunity in chronic gammaherpesvirus infection, including whether the immune system controls latency by regulating latent cell numbers and other properties and what specific immune mediators control latency and persistent replication.
Understanding this complex interplay requires systematic immune monitoring of well characterized human cohorts, but also experimental approaches using primary human cells and genetically modified mouse models. Using these models, we begin to understand the immune recognition of HBV and how it influences the outcome of HBV infection. In this paper we review the current knowledge about virus-host interactions and how it influences the outcome of HBV infection and describe the immune signatures associated with clinical recovery and/or persistent infection.
Vaccination relies on the immune system’s memory of antigens that it encounters, yet our understanding of this fundamental characteristic remains limited. Sprent and Tough discuss current thinking on how memory T cells develop and the various factors that regulate their actions. Some new thoughts on how immune memory is maintained are also offered by Fearon and colleagues, who reason that memory lymphocytes might be akin to self-renewing stem cells that are held in a state of arrested differentiation and perpetual readiness for encounters with antigens.