Identification and molecular characterization of a naturally occurring RNA virus mutant defective in the initiation of host recovery.
The host recovery response is characterized by the disappearance of disease symptoms and activation of the RNA silencing virus resistance in the new growth following an initial symptomatic infection. However, it is not clear what triggers the initiation of recovery, which occurs naturally only in some virus-host interactions. Here we report the identification and characterization of a spontaneous mutant of Tobacco streak virus (TSV) that became defective in triggering recovery in tobacco plants. Infectious full-length cDNA clones corresponding to the tripartite RNA genome were constructed from both the wild-type and the nonrecovery mutant of TSV (TSVnr), the first sets of infectious cDNA clones from an Ilarvirus. Genetic and molecular analyses identified an A --> G mutation in the TSVnr genome that was sufficient to confer nonrecovery when introduced into TSV. The mutation was located in the intergenic region of RNA 3 upstream of the mapped transcriptional start site of the coat protein mRNA. Intriguingly, induction of recovery by TSV was not accompanied by virus clearance and TSV consistently accumulated to significantly higher levels than TSVnr did even though TSVnr-infected plants displayed severe symptoms throughout the course of infection. Thus, our findings indicate that recovery of host can be initiated by minimal genetic changes in a viral genome and may occur in the absence of virus clearance. Mechanisms possibly involved in the initiation of host recovery are discussed.
Xin
Hong-Wu
HW
Molecular Virology Laboratory, Institute of Molecular Agrobiology, National University of Singapore, 1 Research Link, Singapore 117604.
Ding
Shou-Wei
SW
D003001:Cloning, Molecular; D018076:DNA, Complementary / Q000235:genetics; D019179:Ilarvirus / Q000145:classification / Q000235:genetics / Q000472:pathogenicity; D009154:Mutation; D010935:Plant Diseases / Q000821:virology*; D018515:Plant Leaves / Q000821:virology; D012367:RNA, Viral / Q000235:genetics / Q000378:metabolism; D014026:Nicotiana / Q000821:virology*; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism
D018076:DNA, Complementary; D012367:RNA, Viral; D014764:Viral Proteins