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A New Natural Host of Lisianthus necrosis virus in Taiwan

August 2006 , Volume 90 , Number  8
Pages  1,112.3 - 1,112.3

Y. K. Chen and F. J. Jan , Department of Plant Pathology, National Chung Hsing University, Taichung 402, Taiwan ; C. C. Chen , Taichung District Agricultural Improvement Station, Changhua 515, Taiwan ; and H. T. Hsu , Floral and Nursery Plants Research Unit, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, Maryland, 20705



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Accepted for publication 30 May 2006.

Lisianthus necrosis virus (LNV) was first identified as a fungus-borne virus that induced systemic necrosis in lisianthus (Eustoma russellianum) in Japan (2). In Taiwan, LNV causes systemic bright yellow chlorosis followed by necrosis in lisianthus (1). The disease was able to spread through the infested soil. Isolation of a fungus vector was attempted but was not successful (1). Calla lilies (Zantedeschia spp.) showing symptoms of systemic necrosis were observed in the fields of central Taiwan. A virus culture was established through single-lesion isolation from a local lesion host, Chenopodium quinoa, and maintained in Nicotiana benthamiana. Mechanical inoculation of the virus resulted in systemic infection in E. russellianum and Datura stramonium and local infection in Celosia argentea, Gomphrena globosa, Chenopodium amaranticolor, Zinnia elegans, Cucumis melo, Cucumis sativus, Cucurbita pepo, Vigna angularis, and Petunia hybrida. Electron microscopic examination of ultrathin sections of infected plant tissues revealed the presence of spherical viral particles approximately 33 nm in diameter. Scattered and aggregated virion particles were frequently observed in the cytoplasm of infected cells. Results of enzyme-linked immunosorbent assay, western blotting, and immunoelectron microscopy indicate that the virus is serologically related to LNV (1). Reverse transcription-polymerase chain reaction (RT-PCR) with degenerate primers (forward primer 5′-ATGGAAATCGTTAGG and reverse primer 5′-CTATAGCAATGTTGC) for LNV coat protein gene produced a cDNA of approximately 1.1 kb. The RT-PCR product was cloned into pGEM-T vector (Promega, Madison, WI) and sequenced. Sequence analysis showed that the cloned fragment (GenBank Accession No. DQ523229) was 1,167 bp long and shared 99% identity at the nucleotide and deduced amino acid levels with that of the LNV isolated from lisianthus (GenBank Accession No. DQ011234). To our knowledge, this is the first report of the natural occurrence of LNV infection in calla lily.

References: (1) C. C. Chen et al. Plant Dis. 84:506, 2000. (2) M. Iwaki et al. Phytopathology 77:867, 1987.



© 2006 The American Phytopathological Society