The most prevalent in vineyards and well characterised molecularly, but still relatively unknown.

Vast amounts of virus genome sequence data were accumulated recently for viruses infecting grapevines and this trend continues. The reason for this rapid accumulation of data is that the molecular analysis of virus populations in plants is relatively easy. It is just a matter of purifying nucleic acids, amplifying the genome of viruses, sequencing and computer-assisted analysis of obtained sequences. This has led to the development of molecular methods, such as High-Throughput Sequencing (HTS), that precisely evaluate the virus status of investigated grapevines.

Although this is a great achievement from a scientific perspective, the application of these techniques, and revealing that virus infections of grapevines are common in vineyards, cause the average grapevine farmer to become confused and somewhat disappointed. The industry needs solid information on how harmful these viruses are to grapevines. Sometimes this information is lacking and is difficult to obtain. The classical example is grapevine rupestris stem pitting-associated virus (GRSPaV). The discovery of the virus was reported in 1998.1 Soon investigations revealed that GRSPaV is the most widely spread virus in Vitis vinifera vineyards worldwide. Recorded infections amount to 100% of tested grapevines.2 Data from Waite Diagnostics, Australia, suggest that the incidence of the virus differs between various countries: Very high (90.4%) of tested grapevines in Australia, relatively very low in countries like South Africa (14.4%), or, as in Iran, the virus is not present at all.3 However, these rather surprising data need careful investigation. As no insect vector was identified, it is believed that the wide presence of the virus in V. vinifera vineyards is the result of the worldwide exchange GRSPaV-infected grapevines and transmission of this virus by grafting. All tested Iranian samples were collected from native grape cultivars that were growing from their own roots. The very high percentage of GRSPaV infections in vineyards is confusing the grapevine industry. If the GRSPaV infections are common, the intriguing question is, what is the pathogenicity of this virus to grapevines? Should the industry be concerned about this virus? GRSPaV is regarded as being associated with rupestris stem pitting disease (RSPD), which is one of the rugose wood complex diseases (RWD) of grapevines.1 When tissue of a grapevine infected with GRSPaV is grafted to Vitis rupestris cv. St. George plant, symptoms of modified wood (pitting), like that shown in Figure 1, may appear on the woody cylinder of this grapevine. The problem is that the modification of wood is clearly visible only in grapevine V. rupestris cv. St. George, which is especially sensitive to RSPD and is used as an indicator of this disease.


FIGURE 1. Severe RSPD symptoms in Vitis rupestris cv. St. George. GRSPaV status is unknown. (Courtesy of Tobie Oosthuizen, Vititec.)


In other grapevines GRSPaV infections are latent. So what does this mean? Does it mean that the virus does not induce any pathogenic effect in grapevines of these cultivars, but co-exist in peaceful relation with these plants? There are only two papers in which authors address this important question. An Italian laboratory reports that GRSPaV infection triggers various physiological changes in V. vinifera, but it seems these changes would have no negative influence on the productivity of a vineyard.4 The authors suggest that GRSPaV evolved to peacefully co-exist in grapevines. Similar conclusion regarding influence of GRSPaV on grapevine productivity has been reported from Canada.5 However, in both studies little or no attention is given to a detailed characterisation of population of genetic variants of GRSPaV infecting grapevines used in the study. It is well known that not all GRSPaV-infected grapevines grafted to St. George induce RSPD symptoms in this indicator.1

It is believed that the lack of inducing RSPD symptoms in some cases is because of the presence of mild or not pathogenic strains of GRSPaV. Presently eight groups of genetically divergent variants of GRSPaV have been identified.1 The groups are named as GRSPaV-1, -ML, -JF, -PN, -SY, -BS, -SG1 and -SLS. Clear divergence of genome sequences and encoded proteins between members of different groups of GRSPaV suggest that these are different biological strains of this virus, with different pathogenicity to the grapevine host. And this may be true. The laboratory led by Dr. Meng, soon after the discovery of GRSPaV, also discovered that the St. George they used as an indicator of RSPD was already infected with GRSPaV.1 Later they determined that this was a genetic variant GRSPaV-SG1, classified as being not pathogenic to grapevines. Surprisingly, this is the only solid information on pathogenicity of GRSPaV. There is no data on putative severe genetic variants of GRSPaV. In addition, somewhat also surprising is that 22 years after the discovery of GRSPaV, and numerous statements that this virus is associated with RSPD, very little is known about populations of GRSPaV variants inducing clear, severe RSPD symptoms in St. George indicator. Such data, generated in different laboratories, could point to putative severe strains of GRSPaV, which are urgently needed for progress to be made in the study of pathogenicity of this virus in grapevines.


Basically, there are two ways to investigate GRSPaV pathogenicity in controlled laboratory conditions:

  1. Using various natural single infection of grapevines with GRSPaV; or
  2. produce cDNA clone of this ssRNA virus and infect virus-free grapevines using the clone.


Regarding the first option, finding a grapevine infected only with GRSPaV in vineyards may be a serious challenge. However, as the virus is relatively very difficult to eliminate from grapevines, the author believes that single GRSPaV infections can be quickly found in collections of nucleus material of grapevine industries. These grapevines have precise data from RT-PCR testing and woody indexing, and would be excellent for the study. Of special value is the biological data. Genetic heterogeneity of GRSPaV population present in these grapevines could be determined in just a few weeks. Regarding the second option, although the construction of the cDNA clone of GRSPaV is a relatively easy and quick way to obtain a pure culture of any genetic variant of GRSPaV, knowledge of precise events occurring during infection of grapevines by viruses is, in general, still insufficient. To induce the disease, the virus has to successfully infect grapevine cells, increase its titer and systemically spread in a plant. The construction of the cDNA clone of GRSPaV was reported six years ago, in 2013.1 Although it was shown that the clone is infectious to grapevines, the virus was hardly detectable in successfully infected plants. We are still awaiting the report that the GRSPaV originating from such infection is increasing its titer and spreading in grapevine. It may merely be a matter of time since for woody plants, unlike herbaceous hosts, it takes months or years to develop virus infections. Of concern, however, is the fact that the clone is a DNA copy of genetic variant GRSPaV-GG closely related to -SG1 variant, which is putative not pathogenic to grapevines.1 Presently a cDNA clone of another variant, related to GRSPaV-SY, was constructed in the same laboratory. But again, due to insufficient information on the genetic structure of populations of GRSPaV, mentioned earlier in this article, we do not know if the chosen variant is the most likely to be inducing RSPD in St. George.



Grapevine rupestris stem pitting-associated virus (GRSPaV) is the most prevalent virus in vineyards worldwide. Recorded infections of GRSPaV amounts to 100% of tested grapevines. Despite that the virus is well known molecularly, we still do not know much about its pathogenicity to grapevines. It is commonly believed that GRSPaV is a latent pathogen. However, do we really have enough data on putative severe strains of the virus that allow us to make such a statement? The author believes strongly that the industry should invest in further study of this still mysterious virus.



The author thanks Winetech, South Africa for the financial support.



  1. Meng, B. & Rowhani, A., 2017. Grapevine rupestris stem pitting-associated virus. In: Grapevine viruses: Molecular biology, diagnostics and management. Meng, B., Martelli, G.P., Golino, D.E. & Fuchs, M. (eds). Springer, Cham., pp. 257 – 287.
  2. Xiao, H., Shabanian, M., Moore, C., Li, C. & Meng, B., 2018. Survey for major viruses in commercial Vitis vinifera wine grapes in Ontario. Virology Journal 15, 127.
  3. Habili, N., 2015. Failure to detect grapevine rupestris stem pitting-associated virus in Iran may give a clue to the origin of this virus. Proceedings of the 18th Congress of ICVG, Ankara, Turkey, 7 – 11 September 2015, pp. 93 – 94.
  4. Gambino, G., Cuozzo, D., Fasoli, M., Pagliarani, C., Vitali, M., Boccacci, P., Pezzotti, M. & Mannini, F., 2012. Co-evolution between grapevine rupestris stem pitting-associated virus and Vitis vinifera L. leads to decreased defence responses and increased transcription of genes related to photosynthesis. Journal of Experimental Botany 63, 5919 – 5933.
  5. Reynolds, A.G., Lanterman, W.S. & Wardle, D.A., 1997. Yield and berry composition of five vitis cultivars as affected by rupestris stem-pitting virus. American Journal of Enology and Viticulture 48, 449 – 458.


– For more information, contact Dariusz Goszczynski at Plant Health and Protection, Agricultural Research Council –


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