This objective of this research program is to establish the role of interaction between virus defective interfering particles (DIP), infectious standard virus (S-virus) and lymphocytes in the mechanism of virus persistence and dysfunction of the immune system in chronic viral diseases. Results showed that lymphoid tissue of mice acutely or persistently infected with LCMV accumulate high amounts of S-virus and DIP. During the persistent infection, about 3% of the lymphocytes are infected with attenuated mutants of LCMV. Regulatory interactions appear to exist between S-virus, its attenuated mutants and DIP. The specific topics of this investigaton are: a) perisistence of virus in lymphocytes, properties of infected cells as well as of the virus which persists, b) latency of S-virus and DIP in lymphocytes, c) production of DIP in lymphocytes and ability of the latter to support DIP-mediated interference with muliplication of homologous S-virus, e) the effect of infection with S-virus, DIP, or DIP + S-virus on lymphocyte reactivity. The results of this research may add new knowledge regarding the relationship between viruses and lymphocytes, the mechanism of persistent infection, the regulatory function of DIP and their capacity for in vivo prophylaxis, and may also provide a better methodology for the study of virus-lymphocyte interactions in human diseases.
NIH ExPorter
NIH ExPorter