Natural Spread of Cherry Rugose Mosaic Disease and Two Prunus Necrotic Ringspot Virus Biotypes in a Central Washington Sweet Cherry Orchard. W. E. Howell, Scientific Assistant, Department of Plant Pathology, Washington State University, Irrigated Agriculture Research and Extension Center, Prosser 99350. G. I. Mink, Plant Pathologist, Department of Plant Pathology, Washington State University, Irrigated Agriculture Research and Extension Center, Prosser 99350. Plant Dis. 72:636-640. Accepted for publication 16 March 1988. Copyright 1988 The American Phytopathological Society. DOI: 10.1094/PD-72-0636.

The initial appearance and subsequent spread of cherry rugose mosaic (CRM) disease caused by Prunus necrotic ringspot virus (PNRSV) was monitored in a sweet cherry orchard of over 9,000 trees between 1975 and 1986. Between 1975 and 1981, 42 initial disease sites were recognized. Secondary spread occurred at 29 sites despite the fact that diseased trees were usually removed the year that symptoms appeared. Serological tests begun in 1978 detected the presence of another PNRSV biotype that spread at the same rate as the CRM biotype, but that caused no detectable symptoms in cherry trees. These symptomless biotypes were designated HENS (high ELISA, no symptoms). Both CRM and HENS biotypes spread almost exclusively to adjacent trees. The virus spread to an average of only 10% of the adjacent trees each year, and this pattern of spread was not influenced by whether these adjacent trees were pollen compatible or incompatible. Conversely, the probability of CRM spread was greatly reduced by the presence of the HENS biotype, suggesting the natural occurrence of cross-protection between these biotypes. Circumstantial evidence is presented that suggests a relationship between the annual appearance of new CRM sites in the study orchard from 1973 to 1981 and the practice of moving commercial beehives directly from earlier blooming orchards in California to this orchard.