Dissecting the host response to a gamma-herpesvirus.

摘要: The murine gamma-herpesvirus 68 (MHV-68) provides a unique experimental model for dissecting immunity to large DNA viruses that persist in B lymphocytes. analysis is greatly facilitated by the availability of genetically disrupted (-/-) mice lack key host-response elements, and fact MHV-68 lytic virus can readily be manipulated mutational analysis. mutant strategy being used, example, characterize part played vivo an MHV-68-encoded chemokine-binding protein may ultimately find application human therapeutics. Experiments with various -/- monoclonal antibody depletion protocols have shown very clearly type I interferons (IFNs) are essential early control replication, while CD4+ T cells producing IFN-gamma function limit consequences viral persistence. Virus-specific CD8+ effectors acting absence subset seem initially phase lung following respiratory challenge, but then unable prevent reactivation replicative infection epithelia eventual death T-cell-deficient mice. This could reflect interaction between virus-infected targets partially compromised K3 protein, which inhibits antigen presentation MHC class glycoproteins. Immunization strategies focusing on T-cell response epitopes expressed during establishment latency. Other experiments also suggest there disconnection massive nonspecific immunoglobulin dramatic expansion Vbeta4+ cells, apparently independent, represent some sort 'smoke screen' used subvert immunity. Although neither Epstein-Barr nor herpesvirus-8, results generated from this system possibilities usefully addressed these pathogens. Perhaps main lesson learned date all components likely important complex viruses.