3 : Emergence Mechanisms in Yellow Fever and Dengue

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This chapter defines emerging infectious diseases as the diseases which increase or threaten to increase due to genetic changes or to stable changes in microbial trafficking. It considers what is known and unknown about the mechanisms which govern the emergence of yellow fever and the dengue viruses. A succession of genetic studies on yellow fever viruses have concluded that there are at least two or three genotypes in circulation: type I in Central Africa, type IIA in West Africa, and type lIB in the Americas. From clinical reports, dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) can be identified in the medical literature in northeastern Australia in 1897 and continuing for the next fifteen years. The virological attributes of all Asian DHF/DSS epidemics have been the same: (i) multiple types of dengue viruses circulated simultaneously or sequentially and (ii) patients with carefully defined DHF/DSS have secondary-type dengue antibody responses or primary-type responses. In common with other infectious diseases, dengue is characterized by afferent and efferent phases. Afferent events are those phenomena which impact on the survival of microorganisms and their ability to enter cells and replicate. Efferent events are those phenomena which cause illness. Host resistance factors may permanently restrict the penetrance of DHF/DSS into Africa and may already have reduced predicted rates of DHF/DSS morbidity and mortality in the Americas through the widespread distribution of African dengue resistance genes.

Citation: Halstead S. 1998. Emergence Mechanisms in Yellow Fever and Dengue, p 65-80. In Scheld W, Craig W, Hughes J (ed), Emerging Infections 2. ASM Press, Washington, DC. doi: 10.1128/9781555816957.ch3
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Figure 1

Phylogram derived from the nucleotide sequences of the E gene of yellow fever viruses illustrating the evolutionary relationships of genotype I, IIA. and IIIB viruses. The: numbers at the forks indicate the number of times the monophyletic group consisting of viruses to the right of the fork occuned among the 100 trees. (Reprinted with permission from reference )

Citation: Halstead S. 1998. Emergence Mechanisms in Yellow Fever and Dengue, p 65-80. In Scheld W, Craig W, Hughes J (ed), Emerging Infections 2. ASM Press, Washington, DC. doi: 10.1128/9781555816957.ch3
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Illustration of postulated immunopalhogenic events during the two stages of dengue infection. Across the top are shown times after infectious mosquito bite. Cells shown are of the mononuclear phagocyte lineage. C3a. complement breakdown product: IFNγ. interferon gamma: TNFα. tumor necrosis factor alpha; IL. interleukin; Ly. lymphocyte. (Reprinted with permission from reference )

Citation: Halstead S. 1998. Emergence Mechanisms in Yellow Fever and Dengue, p 65-80. In Scheld W, Craig W, Hughes J (ed), Emerging Infections 2. ASM Press, Washington, DC. doi: 10.1128/9781555816957.ch3
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