Abstract:
Grapevine (Vitis vinifera) is susceptible to infections from nearly 70 viruses and virus-like organisms, of which Grapevine leafroll-associated virus 3 (GLRaV-3) is one of the most economically destructive. Infection of GLRaV-3 causes grapevine leafroll disease (GLD), creating characteristic symptoms of leafrolling and chlorosis or leaf reddening, depending on the grapevine cultivar. The extensive genetic variability of the GLRaV-3 viral population has resulted in the classification of isolates into 10 phylogenetic groups. The effect of viral genetic variability on viral titre and spread, virus-encoded suppression of RNA silencing (VSR) activity of p19.6 and p19.7, and symptomology has been investigated in this project using group I, VI and X genetic variants of GLRaV-3. This research has uncovered significant differences in the biological properties of each genetic variant studied, as well as a postulated link between relative VSR activity and virus-titre, spread and symptom development. Group I p19.6 and p19.7 have strong local VSR activities; group I virus has high local accumulation with slow spread. Additionally, group VI p19.6 and p19.7 have possible systemic VSR activities; group VI virus accumulated highly and uniformly throughout the vine, resulting in severe symptoms. Group X p19.6 and p19.7 possess weak local and systemic VSR activities; group X virus has low and slow accumulation and spread with late symptom expression onset. Overall, this work has correlated the role of VSRs in the processes of virus accumulation and spread, symptom patterning and symptom severity from group I, VI and X genetic variants of GLRaV-3. Understanding the pathogenicity factors of GLRaV-3 is a crucial area of research with future implications in mild strain cross-protection. These findings have provided a foundation for future research in obtaining a mild strain of GLRaV-3.
