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ARS Home » Pacific West Area » Corvallis, Oregon » Horticultural Crops Research » Research » Publications at this Location » Publication #198471


item Wegener, L
item Martin, Robert - Bob
item Bernardy, M
item Macdonald, L
item Punja, Z

Submitted to: Canadian Journal of Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/20/2006
Publication Date: 4/1/2007
Citation: Wegener, L.A., Martin, R.R., Bernardy, M.G., Macdonald, L., Punja, Z.K. 2007. Epidemiology and strain identification of Blueberry scorch virus on highbush blueberry in British Columbia. Canadian Journal of Plant Pathology. 28:250.

Interpretive Summary: Blueberry scorch is a devastating disease in many cultivars of highbush blueberry that was first described in 1988 from several fields in Oregon and Washington. Sheep Pen Hill disease, which infects blueberry in New Jersey, was first observed in the 1960's and has since been found to be a strain of Bluberry scorch virus (BlScV). The disease is caused by a virus, BlScV, that is aphid-transmitted in a nonpersistent manner. There has been very limited spread of the virus in Oregon and Washington since it was first discovered. BlScV was first identified in British Columbia, Canada in 2000 and has since been identified in over 140 fields. Since the mid 1990's, the disease has been spreading rapidly in New Jersey and has also been identified in Connecticut, Massachusetts, Italy and the Netherlands. The virus has also been found in cranberry in British Columbia, Oregon and Washington as well as in wild blueberry in British Columbia. Based on sequence information, there is more diversity in BlScV in British Columbia than in the northeastern United States, which suggests that the virus may have originated in native Vaccinium sp in British Columbia and moved from there by people on plant materials.

Technical Abstract: Blueberry scorch virus (BlScV) was first discovered in British Columbia in 2000 and causes a potentially serious disease of highbush blueberry (Vaccinium corymbosum L.). The epidemiology of BlScV was studied over four consecutive years (2001 to 2004) in British Columbia. In 2001, 60 out of 163 blueberry fields sampled tested positive for BlScV using a polyclonal antibody in a double antibody sandwich enzyme-linked immunosorbent assay. In 2002, 79 out of 174 fields sampled tested positive. In 2003, 128 out of 175 fields tested positive and in 2004, 140 out of 227 fields sampled tested positive. Disease spread was studied in more detail by mapping BlScV distribution in three blueberry fields. The percentage increase in diseased plants ranged from 4.4% to 5.2% from 2001 to 2002, and from 4.2% to 9.6% from 2002 to 2004. Symptoms on blueberry cultivars in May included necrosis of blossoms and young leaves, leaf chlorosis and shoot blight; line patterns on the leaves of some infected cultivars were also observed in October. BlScV was also detected in two alternate Vaccinium hosts; cranberry (V. macrocarpon) and wild huckleberry (Vaccinium sp.). Reverse transcription polymerase chain reaction using BlScV-specific primers was used to obtain partial coat protein (CP) sequences of 12 BlScV isolates from British Columbia. A comparison of the CP sequences from the British Columbia isolates with one strain from New Jersey (NJ-2) and two described previously in British Columbia (BC-1, BC-2), revealed that the 12 BC isolates shared 88-100% identity with each other, 87-96% identity with NJ-2, 87-92% identity with strain BC1, and 88-100% identity with strain BC2. The high incidence of BlScV in highbush blueberry in British Columbia and the range of symptoms, the presence of BlScV in alternate hosts, and coat protein sequence variability among strains, suggest that virus spread has been rapid and that different strains of the virus have emerged.