1.13.1S
VECTOR TRANSMISSION OF PLANT VIRUSES: AN OVERVIEW WITH EMPHASIS ON NONCIRCULATIVE TRANSMISSION BY APHIDS

VECTOR TRANSMISSION OF PLANT VIRUSES: AN OVERVIEW WITH EMPHASIS ON NONCIRCULATIVE TRANSMISSION BY APHIDS

TP PIRONE

Department of Plant Pathology, University of Kentucky, Lexington, KY 40546, USA

Background and objectives
Plant viruses have evolved a number of strategies for association with organisms that can provide the wounds necessary for virus inoculation. There are two basic types of relationship between viruses and their most important vectors, insects. Circulative viruses are transported across cell membranes, enter the hemocoel and then the salivary glands, from which they are inoculated. Circulativeviruses can be subdivided into propagative viruses, which replicate in the vector, and nonpropagative viruses, which do not. Non-circulative viruses do not cross membrane barriers but rather are retained in the mouthparts or other regions of the alimentary tract from which they can be inoculated. These same types of relationships could also be applicable for mite- and nematode- transmitted viruses. Viruses transmitted by fungi are borne either externally or internally, depending on the virus. Vector specificity is a hallmark of virus transmission and in this symposium we shall be hearing about some of the complex virus-vector interactions that are involved in the transmission process. Studies in my laboratory focus on the transmission of potyviruses by aphids. Potyvirus transmission requires a transmission competent capsid protein (CP) as well as a functional "helper component" (HC) which is a virally-encoded nonstructural protein. HC functions by acting as a "bridge", interacting with both virions and the food canal of the stylets to allow retention of virions at a site from which they can be inoculated. Below we describe the domains or sites known or proposed to be involved in these interactions.

Results and conclusions
Ultrastructural and autroadiographic studies have shown that successful transmission is always associated with retention of virions within the food canal formed by the maxillary stylets. Furthermore, retention occurs either solely or partially in the distal (i.e. near the tip) portion of the stylets in over 80% of cases [1]. The ability to focus on the stylets has made studies on stylet retention of both virions and HC possible. Changes in the asp-ala-gly "DAG" sequence near the surface-exposed N-terminus of the CP reduce or abolish transmissibility. Aphids fed on mixtures of virions and functional HC retain, in their stylets, vidons having the DAG motif but not those having a DAE motif. Dot-blot binding and protein-blotting overlay assays also reveal a correlation between transmissibility of CP mutants and their ability to bind HC [2]. Mutations in two highly conserved HC motifs result in loss of HC activity. A thr to ala mutation in the conserved PTK motif results in loss of virion- binding ability of HC [3], whereas a lys to glu mutation in the KITC motif results in inability of HC to be retained in the stylets but does not affect binding to virions. The effect of HC on the specificity and efficiency of transmission of the tobacco etch (TEV) and turnip mosaic (TUMV) potyviruses was studied with Myzus persicae, M. ascalonicus, and Lipaphis erysimi. With homologous virion-HC mixtures M. persicae transmitted both TEV and TUMV, L. erysimi transmitted TUMV but not TEV, and M. ascalonicus transmitted neither virus. With heterologous virus-HC mixtures, M. persicae remained a highly efficient vector and M. ascalonicus remained a non-vector, but L. erysimi became an efficient vector of TEV if acquired in the presence of TUMV HC. Transmission was highly correlated with the retention of I151 labeled virions in the stylets. The results show that constituent(s) of or in the food canal of different aphid species differ in the ability to interact with specific HCs, leading to qualitative or quantitative differences in ability to retain and subsequently transmit specific potyviruses.

References
1.Wang RY, Ammar ED, Thornbury DW, Lopez-Moya JJ, Pirone TP, 1996. Journal of General Virology 77, 861-867.
2.Blanc S, Lopez-Moya JJ, Wang RY, Garcia-Lampasona S, Thornbury DW, Pirone T P, 1997. Virology 231, 141-147.
3.Wang Y, Kadoury D, Gal-On A, Huet H, Wang H, Raccah B, 1998. Journal of General Virology (in press).