A general model of plant-virus disease infection incorporating vector aggregation

Citation
Xs. Zhang et al., A general model of plant-virus disease infection incorporating vector aggregation, PLANT PATH, 49(4), 2000, pp. 435-444
Citations number
56
Categorie Soggetti
Plant Sciences
Journal title
PLANT PATHOLOGY
ISSN journal
00320862 → ACNP
Volume
49
Issue
4
Year of publication
2000
Pages
435 - 444
Database
ISI
SICI code
0032-0862(200008)49:4<435:AGMOPD>2.0.ZU;2-2
Abstract
In plant-virus disease epidemiology, dynamical models have invariably incor porated a bilinear inoculation rate that is directly proportional to both t he abundance of healthy (susceptible) hosts and the abundance of infective vectors. Similarly, the acquisition rate is usually assumed to be directly proportional to the abundance of nonviruliferous vectors and that of infect ious hosts. These bilinear assumptions have been questioned for certain hum an diseases, and infection rates that incorporate power parameters of the v ariables have been proposed. Here, infection rates for plant-virus diseases that are of a more general form than the familiar bilinear terms are exami ned. For such diseases, the power parameter can be regarded as a measure of the spatial aggregation of the vectors or as a coefficient of interference between them, depending on the context. Field data of cassava mosaic virus disease (CMD) incidence were examined. W hen vector population density and disease incidence were high, disease prog ress curves over the first 6 months from planting could not be explained us ing models with bilinear infection rates. Incorporation of the new infectio n terms allowed the range of observed disease progress curve types to be de scribed. New evidence of a mutually beneficial interaction between the viru ses causing CMD and the whitefly vector, Bemisia tabaci, has shown that spa tial aggregation of the vectors is an inevitable consequence of infection, particularly with a severe virus strain or a sensitive host. Virus infectio n increases both vector fecundity and the density of vectors on diseased pl ants. It is postulated that this enhances disease spread by causing an incr eased emigration rate of infective vectors to other crops. Paradoxically, w ithin the infected crop, vector aggregation reduces the effective contact r ate between vector and host and therefore the predicted disease incidence i s less than when a bilinear contact rate is used.