Chestnut blight, caused by Cryphonectria parasitica, was identified in Devon, UK, in December 2016. Intensive surveys detected the disease at further sites in Devon (seven), Berkshire (one), Dorset (one), Derbyshire (four) and a cluster of eight sites in southeast London. Over 570 survey samples were tested, and 227 were positive for C. parasitica by isolation and real-time PCR. A total of 227 isolates were tested for mating type, and 197 screened for vegetative compatibility group (VCG) and compared with VCGs known from mainland Europe. The same isolates were also screened for the presence of Cryphonectria hypovirus 1 (CHV-1). Eleven VCGs were identified within the UK population. Five corresponded to already known European VCGs but six were unique. The European VCGs mainly came from the Devon, Dorset, Berkshire and Derbyshire disease outbreaks, whilst unique VCGs were almost exclusively from the southeast London cluster. Both mating types were detected, but only one mating type was present at each site, with the exception of a single Devon site. Perithecia of C. parasitica were never observed at any site. CHV-1 was found in seven isolates from three different locations and was always subtype-I, which has limited hypovirulence. Therefore, although CHV-1 is associated with C. parasitica at some outbreaks, it probably has limited impact on virulence. The diversity of VCGs and their distribution at outbreak sites, together with findings of CHV-1, suggests C. parasitica has been introduced to the UK multiple times over at least two decades through international plant trade.

Chestnut blight is a disease of Castanea species caused by the ascomycete Cryphonectria parasitica. The fungus originates from eastern Asia (Liu et al., 2007) and has little effect on the native host trees Castanea crenata (Japanese chestnut) and Castanea mollisima (Chinese chestnut) (Roane et al., 1986) but it has caused severe epidemics resulting in widespread death and dieback of Castanea dentata (American chestnut) in North America, where the fungus was introduced in the late 19th century (Anagnostakis, 1987), and Castanea

Biological control of Cryphonectria parasitica fungus, causal agent of chestnut blight, by virus infection (hypovirulence) has been shown to be an effective control strategy against chestnut blight in Europe and some parts of North America. The most studied mycovirus is the Cryphonectria hypovirus 1 (CHV-1) type species of the Hypoviridae family. To efficiently provide biocontrol, the virus must be able to induce hypovirulence in its fungal host in chestnut trees. Here, two different CHV-1 subtype I virus strains (E-5 and L-18), gained by transmissions, were tested for their hypovirulence induction, biocontrol potential, and transmission between vegetatively compatible (VCG) and incompatible fungal isolate groups in sweet chestnut seedlings and branches. Both strains of CHV-1 showed great biocontrol potential and could protect trees by efficiently transmitting CHV-1 by hyphal anastomosis between fungal isolates of the same VCG and converting virulent to hypovirulent cankers. The hypovirulent effect was positively correlated with the virus concentration, tested by four different reverse-transcription PCRs, two end-point and two real-time methods, one of which represents a newly developed real-time PCR for the detection and quantification of CHV-1.

Background Chestnut blight, caused by Cryphonectria parasitica, is controlled in many European countries by the naturally occurring mycovirus Cryphonectria hypovirus 1 (CHV‐1). During surveys of recently identified chestnut blight outbreak in England, CHV‐1 was detected in several individuals of the pathogen isolated from affected trees. We investigated two of these CHV‐1‐infected isolates (L‐6 and Db‐1) as potential biocontrol agents for deployment in the UK comparing their virulence against virus‐free (M1275) and hypovirulent (M784) European isolates by inoculating sweet chestnut seedlings. Results Both the European CHV‐1 M784 hypovirulent isolate and UK L‐6 isolate formed significantly smaller lesions in sweet chestnut seedling bark than the other three isolates (Db‐1, and virulent isolates FTC121 and M1275). The highest virus concentration was detected in isolate M784, followed by L‐6, with the lowest concentration in isolate Db‐1. White colony colouration indicative of hypovirulence was common in colonies re‐isolated from smaller lesions, and the same isolates also tended to be slower growing in culture, have a higher virus concentration, and caused less epicormic growth and fewer stromata to be present in plants. L‐6 and Db‐1 virus sequences, respectively, matched the virus haplotype E‐5 detected previously in Switzerland and a mutation of the same subtype I haplotype. Conclusion Isolate L‐6 could potentially act as biocontrol for chestnut blight outbreaks in the UK but further laboratory and field experiments are needed. © 2019 Crown copyright. Pest Management Science © 2019 Society of Chemical Industry

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