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Valero, N. (2003). West Nile virus: a new challenge? Invest Clin, 44(3), 175–177.
Abstract: West Nile Virus (WNV), a member of the family Flaviviridae, was first isolated in 1937. Since the original isolation of the WNV outbreaks have occurred with increase in frequency of cases in humans and horses, apparent increase in severe human disease and high avian death rates. In 1999, 2000 and 2002 outbreaks of the WNV encephalitis were reported in horses, birds and humans from New York and Canada. Ornithophilic mosquitoes are the principal vectors of the WNV and birds of several species chiefly migrants appear to be the major introductory or amplifying host. The pattern of outbreaks in the old and new world suggests that viremic migratory birds may also contribute to movement of the virus. If so, Central America, Caribbean Islands and countries of South America including Venezuela, are in potential risk for suffering a severe outbreak for WNV, since several species of birds have populations that pass trough New York and cross the western north Atlantic or Caribbean Sea. It is important the knowledge of the ecology of WNV as well of the efficacy of control efforts in order to minimize the public health impact in these countries, where all population is susceptible to this infection.
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Hoogstraal, H., & Mitchell, R. M. (1971). Haemaphysalis (Alloceraea) aponommoides Warburton (Ixodoidea: Ixodidae), description of immature stages, hosts, distribution, and ecology in India, Nepal, Sikkim, and China. J Parasitol, 57(3), 635–645.
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Edman, J. D. (1971). Host-feeding patterns of Florida mosquitoes. I. Aedes, Anopheles, Coquillettidia, Mansonia and Psorophora. J Med Entomol, 8(6), 687–695.
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Scherer, W. F., & Dickerman, R. W. (1972). Ecologic studies of Venezuelan encephalitis virus in southeastern Mexico. 8. Correlations and conclusions. Am J Trop Med Hyg, 21(2), 86–89.
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Nosek, J. (1972). The ecology and public health importance of Dermacentor marginatus and D. reticulatus ticks in Central Europe. Folia Parasitol (Praha), 19(1), 93–102.
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Valova, G. P., & Mefod'ev, V. V. (1972). [Specific features of an epidemic process in leptospiroses in northern conditions in Western Siberia]. Zh Mikrobiol Epidemiol Immunobiol, 49(11), 138–145.
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Bast, T. F., Whitney, E., & Benach, J. L. (1973). Considerations on the ecology of several arboviruses in eastern Long Island. Am J Trop Med Hyg, 22(1), 109–115.
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Nelson, W. A., Keirans, J. E., Bell, J. F., & Clifford, C. M. (1975). Host-ectoparasite relationships. J Med Entomol, 12(2), 143–166.
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Wang, L. Y. (1975). Host preference of mosquito vectors of Japanese encephalitis. Zhonghua Min Guo Wei Sheng Wu Xue Za Zhi, 8(4), 274–279.
Abstract: The host preference of 4 Culex mosquito species collected in Miaoli and Pingtung counties, Taiwan was studied by capillary precipitin method. Antisera to alum-precipitated sera of man, bovine, swine, rabbit, horse, dog, cat, mouse, chicken, duck, and pigeon were produced in rabbits and reacted with 758 mosquito blood meals among which reactions to one or more antisera. Culex annulus and Culex tritaeniorhynchus summorosus showed a great avidity for pig, and Culex fuscocephala for bovine. Culex pipiens fatigans was ornithophilic. None of 110 C. t. summorosus and 2.4% of 223 C. annulus had fed on man. Among 66 samples of C.p. fatigans tested 10.3% had fed on man, while none of 359 C. fuscocephala did. It seems that the latter does not act as a primary vector of Japanese encephalitis.
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Dowdle, W. R., & Schild, G. C. (1976). Influenza: its antigenic variation and ecology. Bull Pan Am Health Organ, 10(3), 193–195.
Abstract: Influenza viruses have two surface antigens, the glycoprotein structures hemagglutinin (HA) and neuraminidase (NA). Antibodies to each of these are associated with immunity, but the structures themselves are antigenically variable. When an antigenic change is gradual over time it is referred to as a drift, while a sudden complete or major change in either or both antigens is termed a shift. The mechanism of antigenic drift is usually attributed to selection of preexisting mutants by pressure from increasing immunity in the human population. The mechanism of antigenic shift is less clear, but one tentative hypothesis is that shifts arise from mammalian or avian reservoirs, or through genetic recombination of human and animal influenza strains.
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