|Karasev, Alexander - UNIV. OF FLORIDA|
|Dawson, William - UNIV. OF FLORIDA|
Submitted to: Acta Horticulturae
Publication Type: Review Article
Publication Acceptance Date: June 5, 1997
Publication Date: N/A
Interpretive Summary: Not required.
Technical Abstract: Citrus tristeza virus (CTV) causes a complex of disease syndromes in Citrus spp., the two most important syndromes are decline of trees propagated on sour orange rootstock, and stem-pitting in susceptible scions which occurs in decline-tolerant cultivars irrespective of the scion-rootstock combination. The 2,000 nm-long virion of CTV is composed of a single positive-sense RNA molecule of 19,296 nt and a major capsid protein (CO) of 25-kDa. The genome of CTV encompasses 12 open reading frames (ORFs) which code for at least 19 protein products ranging from 6 to 401-kDa. The mode of expression of the CTV genome combines proteolytic processing of the polyprotein precursor, translational frameshifting, and formation of subgenomic RNAs. CTV represents a very complex genetic system and infected plants contain the genomic RNA, at least nine subgenomic RNAs, and often multiple defective RNAs. In many cases plants are doubly or multiply infected with genetically distinct CTV isolates or strains, and there are indications of high recombination potential between different virus-specific RNAs. Molecular genetic analysis revealed substantial sequence heterogeneity, of up to 40% between different isolates, in certain regions of the CTV genome. Initial attempts to link certain sequences of the CTV genome to a particular symptomatology were largely unsuccessful, probably due to the lack of information concerning the mechanisms of the CTV pathogenesis. Further work on pathogen-derived resistance to CTV, mild strain cross-protection, detection and differentiation of CTV isolates, and formulation of control strategies, may greatly benefit from the studies of the CTV molecular biology.