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Open AccessJournal ArticleDOI

Weather, host and vector — their interplay in the spread of insect-borne animal virus diseases

R. F. Sellers
- 01 Aug 1980 - 
- Vol. 85, Iss: 1, pp 65-102
TLDR
The spread of insect-borne animal virus diseases is influenced by a number of factors, and it is preferable to protect the host by dipping, spraying or by vaccination rather than attempting to eliminate the local population of insects.
Abstract
The spread of insect-borne animal virus diseases is influenced by a number of factors. Hosts migrate, move or are conveyed over long distances: vectors are carried on the wind for varying distances in search of hosts and breeding sites; weather and climate affect hosts and vectors through temperature, moisture and wind. As parasites of host and vector, viruses are carried by animals, birds and insects, and their spread can be correlated with the migration of hosts and the carriage of vectors on winds associated with the movements of the Intertropical Convergence Zone (ITCZ) and warm winds to the north and south of the limits of the ITCZ. The virus is often transmitted from a local cycle to a migratory cycle and back again.Examples of insect-borne virus diseases and their spread are analysed. Japanese, Murray Valley, Western equine, Eastern equine and St Louis encephalitis represent viruses transmitted by mosquito-bird or pig cycles.THE AREAS EXPERIENCING INFECTION WITH THESE VIRUSES CAN BE DIVIDED INTO A NUMBER OF ZONES: A, B, C, D, E and F. In zone A there is a continuous cycle of virus in host and vector throughout the year; in zone B, there is an upsurge in the cycle during the wet season, but the cycle continues during the dry season; there is movement of infected vectors between and within zones A and B on the ITCZ and the virus is introduced to zone C by infected vectors on warm winds; persistence may occur in zone C if conditions are right. In zone D, virus is introduced each year by infected vectors on warm winds and the arrival of the virus coincides with the presence of susceptible nestling birds and susceptible piglets. The disappearance of virus occurs at the time when migrating mosquitoes and birds are returning to warmer climates. The virus is introduced to zone E only on occasions every 5-10 years when conditions are suitable. Infected hosts introduced to zone F do not lead to circulation of virus, since the climate is unsuitable for vectors. Zones A, B and C correspond to endemic and zones D and E to epidemic conditions.Similar zones can be recognized for African horse sickness, bluetongue, Ibaraki disease and bovine ephemeral fever - examples of diseases transmitted in a midge-mammal cycle. In zones A and B viruses are transported by infected midges carried on the wind in association with the movement of ITCZ and undergo cycles in young animals. In these zones and in zone C there is a continual movement of midges on the warm wind between one area and another, colonizing new sites or reinforcing populations of midges already present. Virus is introduced at times into fringe areas (zones D and E) and, as there is little resistance in the host, gives rise to clinical signs of disease. In some areas there is persistence during adverse conditions; in others, the virus is carried back to the endemic zones by infected midges or vectors.Examples of viruses maintained in a mosquito/biting fly-mammal cycle are Venezuelan equine encephalitis and vesicular stomatitis. These viruses enter a migratory cycle from a local cycle and the vectors in the migratory cycle are carried over long distances on the wind. Further examples of virus spread by movement of vectors include West Nile, Rift Valley fever, yellow fever, epizootic haemorrhagic disease of deer and Akabane viruses.In devising means of control it is essential to decide the relationship of host, vector and virus and the nature of the zone in which the area to be controlled lies. Because of the continual risk of reintroduction of infected vectors, it is preferable to protect the host by dipping, spraying or by vaccination rather than attempting to eliminate the local population of insects.

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Citations
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Present and future arboviral threats.

TL;DR: Viruses such as dengue (DENV) and chikungunya (CHIKV) that have lost the requirement for enzootic amplification now produce extensive epidemics in tropical urban centers, and climate warming could facilitate the expansion of the distributions of many arboviruses.
Journal ArticleDOI

Culicoides biting midges: their role as arbovirus vectors.

TL;DR: Those aspects of midge biology facilitating disease transmission are dealt with, the factors controlling insect-virus interactions at the individual insect and population level are described, and the far-reaching effects that certain components of climate have upon the midges and, hence, transmission potential are illustrated.
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Impact of climate change and other factors on emerging arbovirus diseases

TL;DR: The question is asked, are these diseases emerging because of climate change or do other factors play an equal or even more important role in their emergence?
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Ecology and Geographical Expansion of Japanese Encephalitis Virus

TL;DR: The ecology of JEV is outlined and the recent expansion of its geographical range is examined, before assessing its ability to emerge in new regions, using the hypothetical establishment in the United States as a case study.
Journal ArticleDOI

Landscape epidemiology of vector-borne diseases.

TL;DR: The evolution of landscape epidemiology is described as a science and exemplifies selected aspects by contrasting the ecology of two different recent disease outbreaks in North America caused by West Nile virus, an explosive, highly virulent mosquito-borne virus producing ephemeral nidi, and Borrelia burgdorferi, a slowly amplifying chronic pathogen producing semipermanent nidi.
References
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Journal ArticleDOI

World Survey of Climatology

Reid A. Bryson, +1 more
- 01 Oct 1975 - 
Journal ArticleDOI

Measles endemicity in insular populations: Critical community size and its evolutionary implication

TL;DR: It is postulated that populations sufficient to support continued propagation of this virus did not exist in primitive societies and that measles virus must have evolved since the development of early civilizations.
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