Tiollier, V. 1980. Vanilla cultivation in Tonga. Technical Bulletin 1:37.
Tiollier, V. 1983. Vanilla curing in Tonga. Technical Bulletin 5:73.
Wong, C., Wong, M., and Grisoni, M. 2003. Culture de la vanilla. Fiches techniques/technical leaflets, 37pp. (audiovisual material).
Chapter 7. Virus Diseases of Vanilla
Michel Grisoni, Michael Pearson, and Karin Farreyrol
Virus diseases became a major concern for vanilla production over the last few decades probably as a consequence of the diversification of the cultivation areas and intensification of vanilla growing. This chapter reviews the data accumulated on the viruses affecting vanilla plantation throughout the world, particularly Cymbidium mosaic virus (CymMV), potyviruses, and Cucumber mosaic virus (CMV). It discusses how the environmental changes induced by the intensification of vanilla cultivation have favored the emergence of viral epidemics, the possible control strategies available at present, and the research perspectives to improve them.
Introduction
Viruses are obligatory cellular parasites that can infect bacteria, fungi, plants, and animals. They have probably emerged and evolved in their hosts at the beginning of the tree of life (Forterre, 2006). Virus particles are basically made of one or few genomic ribonucleic acid (RNA) or deoxyribonucleic acid (DNA) molecules encapsulated in a protein shell, the capsid. More than 5000 virus species are currently recognized (Fauquet et al., 2005), of which ~1000 infect plants and have been classified into more than 60 genera (Wren et al., 2006). Most of them are disease causing since virus development induces symptoms in host tissues that may generate severe crop losses. Plant viruses are only infrequently transmitted by seeds but somatic plant parts such as cuttings, bulbs, and buds ensure the propagation of many plant viruses. Horizontal transmission of viruses often involves animal vectors (mostly insects), but some viruses have no vector and only infect new hosts by contact with epidermal wounds.
More than 20 virus species have been reported to infect orchids (Gibbs and Mackenzie, 1997). The first demonstration of vanilla infection by a virus was by Wisler et al. (1987), in French Polynesia (FP). To date 10 virus species belonging to four families of positive-sense RNA genome viruses have been described from vanilla.
Cymbidium Mosaic Virus (Cymmv)
CymMV is the most prevalent and economically damaging virus infecting orchids (Zettler et al., 1990). Since its first description by Jensen in California (Jensen, 1950; Jensen and Gold, 1955), CymMV has been reported in most cultivated orchid species in many countries and is now considered to be present worldwide. CymMV was first detected in vanilla during a survey in FP (Wisler et al., 1987). It was subsequently found in vanilla plots of many countries: Cook Islands, Fiji, Niue, and Tonga (Pearson et al., 1993), Madagascar (Grisoni et al., 1997), Reunion Island (Pearson, 1997), Mauritius (Rassaby, 2003), India (Bhat et al., 2006) as well as in material conserved in botanical gardens (Grisoni et al., 2007).
Virus Structure and Genetic Diversity
As a member of the genera Potexvirus, family Flexiviridae (Adams et al., 2004), CymMV has flexuous particles (~13 nm × 480 nm) containing a single-stranded RNA (+) genome of about 6.3 kb with five open reading frames (ORFs) flanked by 5′ and 3′ noncoding regions plus a 3′ polyA tail (Francki, 1970; Wong et al., 1997).
The GenBank database contained (in October 2009) the complete genome sequence for nine isolates of CymMV and over 100 sequences for the coat protein (CP) gene, most of which are of Asian origin. The overall diversity between isolates is low at the amino acid level, with less than 14% divergence for CP (Ajjikuttira et al., 2002; Bhat et al., 2006; Gourdel and Leclercq-Le Quillec, 2001; Moles et al., 2007; Sherpa et al., 2006) and less than 3% divergence for RNA-dependent RNA polymerase (Moles et al., 2007). Nucleotide sequence analyses revealed, however, that the CymMV population splits into two diverging haplogroups, which may reflect a dual origin for the isolates found worldwide. However, no biological difference has been observed between the two clusters of strains, which can coexist and recombine within the same host (Sherpa et al., 2007; Vaughan et al., 2008). Strains belonging to both CymMV subgroups have been found in vanilla (Moles et al., 2007).
Symptoms and Diagnosis
In ornamental orchids, CymMV causes chlorotic or necrotic spots and streaks on leaves and flowers (Albouy and Devergne, 1998; Gibbs et al., 2000; Yamane et al., 2008) and reduces plant growth (Izaguirre-Mayoral et al., 1993; Pearson and Cole, 1991; Wannakrairoj, 2008). In vanilla, CymMV infection is generally symptomless but has occasionally been associated with flecking on leaves (on Vanilla planifolia and Vanilla tahitensis) and necrotic spots on the stem and leaves (on V. planifolia) (Grisoni et al., 1997, 2004; Leclercq Le Quillec et al., 2001) (Figure 7.1). It has been suggested from field observations that CymMV weakens the vine and increases decline due to stresses, resulting from overcropping or infection with another pathogen (Benezet et al., 2000), but this remains to be demonstrated. Even in the absence of symptoms, CymMV infection can be responsible for up to 40% reduction of stem growth (Bartet, 2005). The impact of CymMV on aromatic content of the pods has not been investigated so far.
FIGURE 7.1 (See color insert following page 136.) Chlorotic (left) and necrotic (right) flecks induced by CymMV on vanilla leaves.
Observations in field surveys indicated that CymMV symptoms were more severe on V. planifolia (in Indian Ocean area) than on V. tahitensis (in the Pacific). The evaluation of disease severity in comparable greenhouse conditions using a local subgroup A strain in Reunion Island did not show any difference in virus disease between these two Vanilla species. Surprisingly however, a Vanilla pompona accession included in the trial exhibited partial resistance to this virus. This resistance consisted of two components: (1) resistance to inoculation (lower rate of infected plants in mechanical inoculation tests compared to V. tahitensis and V. planifolia accessions, and (2) reduction of virus titer in the infected leaves, resulting several months after inoculation with apparent elimination of the virus (Table 7.1). This resistance evokes transient inhibition of posttranscriptional gene silencing by CymMV in V. pompona rather than a hypersensitive response (Baures et al., 2008), but the mechanism underlying this resistance is unclear and needs further investigation.
| Species-Accession | Proportion of Infected Plants | |||
|---|---|---|---|---|
| Exp 1 | Exp 2 | Exp 3 | Average (%) | |
| V. pompona–CR0018 | 5/12 | 4/10 | 0/20 | 21 |
| V. pompona–CR0031 | Nd | 4/10 | 6/28 | 26 |
| V. planifolia–CR0044 | 13/13 | 10/10 | 42/48 | 92 |
| V. planifolia–CR0036 | 12/12 | 10/10 | 36/40 | 93 |
| V. tahitensis–CR0017 | 10/10 | 10/10 | Nd | 100 |
| V. bahiana–CR0087 | Nd | 7/10 | Nd | 70 |
| V. crenulata–CR0091 | Nd | 10/10 | Nd | 100 |