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Virol J. 2008; 5: 9.
Published online 2008 January 16. doi: 10.1186/1743-422X-5-9.
PMCID: PMC2244595
Genetic variation and recombination of RdRp and HSP 70h genes of Citrus tristeza virus isolates from orange trees showing symptoms of citrus sudden death disease
Clarissa PC Gomes,1 Tatsuya Nagata,corresponding author1 Waldir C de Jesus, Jr,2,5 Carlos R Borges Neto,3 Georgios J Pappas, Jr,1 and Darren P Martin4
1Programa de Pós-Graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília. SGAN, Quadra 916, Módulo B, Av. W5 Norte, 70.790-160, Brasília-DF, Brazil
2Fundecitrus, Av. Adhemar Pereira de Barros, 201, 14807-040, São Paulo, SP, Brazil
3CENARGEN, Parque Estação Biológica, Av. W5 Norte, 70770-900, Brasília, DF, Brazil
4Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, Cape Town, 7000, South Africa
5Universidade Federal do Espírito Santo, Centro de Ciências Agrárias, Alto Universitário, S/N, 29500-000, ES, Brazil
corresponding authorCorresponding author.
Clarissa PC Gomes: clarissagomes/at/yahoo.com.br; Tatsuya Nagata: tatsuya/at/pos.ucb.br; Waldir C de Jesus, Jr: wcintra/at/yahoo.com; Carlos R Borges Neto: cborges/at/cnpq.br; Georgios J Pappas, Jr: gpappas/at/pos.ucb.br; Darren P Martin: Darrin.Martin/at/uct.ac.za
Received December 17, 2007; Accepted January 16, 2008.
Abstract

Background
Citrus sudden death (CSD), a disease that rapidly kills orange trees, is an emerging threat to the Brazilian citrus industry. Although the causal agent of CSD has not been definitively determined, based on the disease's distribution and symptomatology it is suspected that the agent may be a new strain of Citrus tristeza virus (CTV). CTV genetic variation was therefore assessed in two Brazilian orange trees displaying CSD symptoms and a third with more conventional CTV symptoms.

Results
A total of 286 RNA-dependent-RNA polymerase (RdRp) and 284 heat shock protein 70 homolog (HSP70h) gene fragments were determined for CTV variants infecting the three trees. It was discovered that, despite differences in symptomatology, the trees were all apparently coinfected with similar populations of divergent CTV variants. While mixed CTV infections are common, the genetic distance between the most divergent population members observed (24.1% for RdRp and 11.0% for HSP70h) was far greater than that in previously described mixed infections. Recombinants of five distinct RdRp lineages and three distinct HSP70h lineages were easily detectable but respectively accounted for only 5.9 and 11.9% of the RdRp and HSP70h gene fragments analysed and there was no evidence of an association between particular recombinant mosaics and CSD. Also, comparisons of CTV population structures indicated that the two most similar CTV populations were those of one of the trees with CSD and the tree without CSD.

Conclusion
We suggest that if CTV is the causal agent of CSD, it is most likely a subtle feature of population structures within mixed infections and not merely the presence (or absence) of a single CTV variant within these populations that triggers the disease.