Citrus tristeza virus: a pathogen that changed the course of the citrus industry

Abstract

Citrus tristeza virus (CTV) (genus Closterovirus, family Closteroviridae) is the causal agent of devastating epidemics that changed the course of the citrus industry. Adapted to replicate in phloem cells of a few species within the family Rutaceae and to transmission by a few aphid species, CTV and citrus probably coevolved for centuries at the site of origin of citrus plants. CTV dispersal to other regions and its interaction with new scion varieties and rootstock combinations resulted in three distinct syndromes named tristeza, stem pitting and seedling yellows. The first, inciting decline of varieties propagated on sour orange, has forced the rebuilding of many citrus industries using tristeza-tolerant rootstocks. The second, inducing stunting, stem pitting and low bearing of some varieties, causes economic losses in an increasing number of countries. The third is usually observed by biological indexing, but rarely in the field. CTV polar virions are composed of two capsid proteins and a single-stranded, positive-sense genomic RNA (gRNA) of approximately 20 kb, containing 12 open reading frames (ORFs) and two untranslated regions (UTRs). ORFs 1a and 1b, encoding proteins of the replicase complex, are directly translated from the gRNA, and together with the 5' and 3'UTRs are the only regions required for RNA replication. The remaining ORFs, expressed via 3'-coterminal subgenomic RNAs, encode proteins required for virion assembly and movement (p6, p65, p61, p27 and p25), asymmetrical accumulation of positive and negative strands during RNA replication (p23), or suppression of post-transcriptional gene silencing (p25, p20 and p23), with the role of proteins p33, p18 and p13 as yet unknown. Analysis of genetic variation in CTV isolates revealed (1) conservation of genomes in distant geographical regions, with a limited repertoire of genotypes, (2) uneven distribution of variation along the gRNA, (3) frequent recombination events and (4) different selection pressures shaping CTV populations. Measures to control CTV damage include quarantine and budwood certification programmes, elimination of infected trees, use of tristeza-tolerant rootstocks, or cross protection with mild isolates, depending on CTV incidence and on the virus strains and host varieties predominant in each region. Incorporating resistance genes into commercial varieties by conventional breeding is presently unfeasible, whereas incorporation of pathogen-derived resistance by plant transformation has yielded variable results, indicating that the CTV-citrus interaction may be more specific and complex than initially thought. A deep understanding of the interactions between viral proteins and host and vector factors will be necessary to develop reliable and sound control measures.

Evidence of Recombinant Citrus tristeza virus Isolate Occurring in Acid Lime cv. Pant Lemon Orchard in Uttarakhand Terai Region of Northern Himalaya in India

“…Isolate Pant 4 showed 99-100 % aa sequence identity with Kpg3 for ORF7, 9 and 10, indicating both the isolates are similar in pathogenecity, ORF7 encodes for major CP and RNAi suppressor, ORF9 for p13 protein with unknown function and ORF10 for RNAi suppressor [17]. ORF encodes p18 protein the function of which is unknown [17]; ORF8 of Pant 4 is different from Kpg3 isolate, indicating that p18 might have role in host specificity as Rough lemon is infected by the isolate Kpg3 in the Darjeeling hills but not by the isolate Pant 4 in glass conditions. A close relationship in amino acid sequence (99-100 % identity) of isolates Pant 4 and Kpg3 with Hawaii isolate HA16-5 for ORF7 and 9 was observed, that indicated both the Indian isolates might be related to Hawaii isolate in pathogenecity.…”

“…It is interesting to note that even under highly favourable environmental condition that All position containing gaps and missing data were eliminated from the dataset using complete deletion option n nucleotide expansion, m number of isolates those were used in phylogenetic analysis, S number of segregation sites, p s S divided by n, h population mutation rate, p pair wise nucleotide diversity by the average number of differences per site between two sequences, D Tajima [19]. Isolate Pant 4 showed 99-100 % aa sequence identity with Kpg3 for ORF7, 9 and 10, indicating both the isolates are similar in pathogenecity, ORF7 encodes for major CP and RNAi suppressor, ORF9 for p13 protein with unknown function and ORF10 for RNAi suppressor [17]. ORF encodes p18 protein the function of which is unknown [17]; ORF8 of Pant 4 is different from Kpg3 isolate, indicating that p18 might have role in host specificity as Rough lemon is infected by the isolate Kpg3 in the Darjeeling hills but not by the isolate Pant 4 in glass conditions.…”

Evaluation of the protective capacity of new mild Citrus tristeza virus (CTV) isolates selected for a preimmunization program

“…However, other isolates were altered after being challenged by the severe isolate by grafting or vector inoculation. Because several authors indicated haplotype selection after aphid transmission (Broadbent et al, 1996;Sambade et al, 2002;Moreno et al, 2008), it was assumed that the tissue union would be more effective for transmitting the challenging virus than the vector inoculation (Müller and Rezende, 2004). However, in some cases, and for the plants maintained under screens, the inoculation of the challenging isolate was more effective with brown citrus aphid.…”

“…The risks of spreading these severe isolates to new areas by propagation or nursery trees are real and should be considered (Herrera-Isidrón et al, 2009). Therefore, losses can only be effectively reduced and prevented by an efficient system of preimmunization against these severe isolates (Sambade et al, 2002;Moreno et al, 2008). Recent studies point to the existence of severe CTV isolates in the northern regions of Paraná state, Brazil.…”

Citrus tristeza virus infection induces the accumulation of viral small RNAs (21–24-nt) mapping preferentially at the 3′-terminal region of the genomic RNA and affects the host small RNA profile

“…(Albiach-Martí et al 2010). In nature CTV infection is restricted to phloem cells of som e species of tw o genera of the fam ily Rutaceae (Moreno et al 2008), with the virus reaching variable titers d epend ing on the strain and the host: the titer in Mexican lim e (C. aurantifolia (Christm .) Swing.)…”