Viral pathogenesis and resistance to defective interfering particles

摘要: Recently presented evidence indicates that synthesis of defective interfering (DI) particles following infection cultured cells with lymphocytic choriomeningitis (LCM) virus may result in self-curing1. The genesis DI can occur infected virtually any animal virus2, and seems to be a host-controlled function3. Thus, these represent third line defence—with the immune response interferon—against invasion3,4. LCM causes rapid appearance tissue culture cells5,6. Nevertheless, persistent infections easily established other arenaviruses7–9. LCM-persistent are apparently maintained cultures by DI-resistant viruses1. This latter finding prompted us determine whether such viruses nature. Vertical transmission house mouse or neonatal laboratory mice takes form life-long inap-parent infection. These lack functional virus-specific T lymphocytes, but make an antibody against invasion. It is known injected into change during course so at least two different viral populations coexist same mouse10. produced abundance shortly after this precedes population that, plaque morphology, differs from one originally inoculated11. We report here isolation persistently resistant not only which were heterotypic also itself induces neonates. know no replicate normally presence they induce.