beet leafhopper in the spread and development of sugar beet curly top disease in Utah. However, he did not attribute the appearance of the disease to any viral or pathogenic entity, figuring that the damage was directly caused by the feeding injury induced by the insect. It was not until 1915 that the relationship between the vector and the virus in causing disease was irrefutably established by P. A. Boucquet and W. J. Hartung. They showed that after leafhoppers taken from the wild with no previous contact with sugar beets were allowed to feed on beets, no disease ensued. But when they were allowed to feed on beets with symptoms of curly top for 3–7 days, curly top symptoms appeared on previously healthy beets after leafhoppers were transferred and granted time to feed. The discovery of curly top transmission by leafhoppers strongly suggested a viral etiology; however, the pathogen's identity was not formally established until the 1970s. The typically low concentration of virus particles within infected plants made isolation and purification difficult. Therefore, it was not until 1974 that a virus was formally proven to be the cause of the disease, after advancements in virus purification were made and the characteristic twinned particles of geminiviruses were observed with electron microscopy. Strains There are many strains of curly top virus. They are CA/Logan = California/Logan, CO = Colorado, Kim1 = Kimberly1, LH71 = Leafhopper 71, Mld = Mild, PeCT = Pepper curly top, PeYD = Pepper yellow dwarf, Svr = Severe (formerly CFH), SvrPep = Severe pepper, SpCT = Spinach curly top, and Wor = Worland. Structure and replication The genome of curtoviruses consists of a single circular ssDNA component of 2.9–3.0 kb, encoding six to seven proteins. The three ORFs encoded on the virion-sense strand are the coat protein (CP, ORF V1), which encapsidates the virion-sense ssDNA and is involved in virus movement and insect vector transmission, a movement protein (MP, ORF V2), and V3, which is involved in the regulation of the relative levels of ssDNA and dsDNA. The complementary-sense strand encodes the replication-associated protein (Rep, ORF C1), which is required for the initiation of viral DNA replication, the C2 protein (ORF C2), which acts as a pathogenicity factor in some hosts, a replication enhancer protein (REn, ORF C3), and the C4 protein (ORF C4), which is an important symptom determinant implicated in cell-cycle control (Hanley-Bowdoin et al., 2013).