A novel type of defective viral genome suggests a unique strategy to establish and maintain persistent lymphocytic choriomeningitis virus infections.
Defective interfering RNAs have long been thought to be a causal factor of persistent RNA virus infections. Here we describe a novel type of defective genome of lymphocytic choriomeningitis virus and the unique mechanism by which these RNAs appear to contribute to the establishment and maintenance of persistent infection. The defective genomes have short deletions in the untranslated regions at their termini and additional nontemplated terminal nucleotides. This and previous work from our laboratory suggested that the RNAs were competent for replication but not for transcription. From experiments using a technique to unambiguously determine the sequences of individual RNA termini, it appears that some truncated RNAs can be repaired. The data suggest that the loss or gain of nucleotides from the RNA termini during the course of infection is the mechanism for establishing and maintaining persistence.
Meyer
B J
BJ
Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455, USA.
Southern
P J
PJ
D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D003673:Defective Viruses / Q000235:genetics* / Q000502:physiology; D016679:Genome, Viral; D008216:Lymphocytic Choriomeningitis / Q000821:virology*; D008217:Lymphocytic choriomeningitis virus / Q000235:genetics* / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D012367:RNA, Viral / Q000235:genetics / Q000502:physiology; D013698:Templates, Genetic
D012367:RNA, Viral