![Immunology and Pathogenesis of Dengue Pathogenesis: Two Theories [Immunological & Virological theories]. Replication in a number of cells: Macrophages, Monocytes , B cells, mast cells, Dendritic cells, Endothelial cells. Viral entry: Fc-gamma receptors of the host cells. Fc-gamma: Implicated in ADE. The genetic determinants on E gene and the 5’ and 3’ untranslated regions (The viral Theory). Dengue virus reactive T-cells: React differently with various serotypes. Multiplicity of Genetic determinants.](https://image.slidesharecdn.com/biologicalcontrolofdengue-111025092200-phpapp02/75/Biological-control-of-dengue-8-2048.jpg)
![Pathogenesis of Dengue Host genetic + Environmental + Viral factors Absence of an animal model of disease: Candidate genes Identification for Susceptibility and Resistance. Host Genetics: Variability at HLA I loci, Fc-gamma, Vit D receptor, promoter region of CD209 ---- Associated with distinct symptomatic phenotypes. Host Immune pressure: Disease outcome + Viral evolution [within individual (quasispecies), or at geographic scale]. Expression of special class I alleles: Associated with outcome.](https://image.slidesharecdn.com/biologicalcontrolofdengue-111025092200-phpapp02/75/Biological-control-of-dengue-9-2048.jpg)
![Immunology of Dengue Antibody Dependant Enhancement [IgG not IgM]. DEN1 (X Individual) ------ Ab (Anti-DEN1): [Life long Immunity] Ag:Ab complex (No entry into macrophages) DEN 2/3/4 (X) ---- Activation of Immune system [Takes it for the primary infection] Higher genetic similarity [ Similar surface proteins ]: The Immune system is tricked. Ab:Ag complexes [ No inactivation of the Ag ] Macrophages are attracted and infected : Sever consequences, infection becomes more acute, body releases cytokines [makes endothelial tissue more permeable] ------ DHF and Fluid loss . Vaccination & Passive acquisition of Abs in childern would have the same consequences.](https://image.slidesharecdn.com/biologicalcontrolofdengue-111025092200-phpapp02/75/Biological-control-of-dengue-11-2048.jpg)
![Control Strategies Control of Immature stages: Vector control [Larviciding with insecticides, elimination of breeding sites] Only temephos, permethrin, Bti, and pyriproxyfen are approved by WHO for use in drinking-water. Pyriproxyfen: Effective, new formulations are effective for 6 months, 1 ppb. Decrease fertility in adults. Limitations: Prevents only eclosion, Larvae and Pupae are active. BTi Toxins: Bacillus thuringiensis var. israelensis (Bti) High larvicidal activity in mosquitoes. Limitations: Combinations: BTi + Insecticide, BTi + Copepods: Effective but needs persistent follow up and supplementary food is needed. Others: Insecticide treated materials, Lethal ovitraps at airports.](https://image.slidesharecdn.com/biologicalcontrolofdengue-111025092200-phpapp02/75/Biological-control-of-dengue-12-2048.jpg)
![Control Strategies Mechanism of the cross: Transformation of the Mosquito Population Female Infected [ Wol+ ] X Male [Wild type] = Infected M/F. Female [ Wild type ] X Male [ Infected Wol+ ] = Sterile Eggs.](https://image.slidesharecdn.com/biologicalcontrolofdengue-111025092200-phpapp02/75/Biological-control-of-dengue-15-2048.jpg)
Uploaded byHamid Ur-Rahman
Biological control of dengue
There are four serotypes of the dengue virus that are transmitted to humans by the Aedes mosquito. While dengue fever causes mild illness, dengue hemorrhagic fever and dengue shock syndrome can be deadly if left untreated. Current control strategies focus on reducing mosquito populations through larvicide use and eliminating breeding sites, but novel biological approaches are being explored including using Wolbachia bacteria to transform mosquito populations or predator copepods. Further research continues into viral genetics and host immunology to better understand disease pathogenesis and identify new treatment targets.
More Related Content
Similar to Biological control of dengue
Biological control of dengue
- 1. Biological Control ofDengue Dr. Ijaz Ali IBGE SAPCID
- 2. Introduction Dengue VirusDengue Vectors Immunology of Dengue Dengue Control Programs Dengue Biological Control Some Concerns Active Research Areas
- 3. The Dengue VirusDengue Fever: First reported in 1779. Dengue Hemorrhagic Fever (DHF): 5% mortality. Dengue Shock Syndrome (DSS): 40% mortality. Flaviviridae; 70 members, Major cause of pathologies in human/animals. Flavivirus (Human), Pestvirus (Animals), Hepacivirus. Follow climatic events. Arbovirus: Replicates both in vertebrates & invertebrates. Category A pathogen. 10.5 kb Genome: 96 Whole Genome Sequences. Four Serotypes: DEN1-4. 60-80% sequence homology. Surface Protein Homology. Problems with RNA Genomes: Frequent Mutations. DEN2: The Asian American type causes DHF but the American type cause DHF in secondary infections.
- 4. The Virus SriLanka: Genetically distinct DEN3 with variable virulence. Strains isolated before 1989: No DHF. DEN4 causes less sever disease.
- 5. Dengue Vectors TheAedes Mosquito Aedes aegypti: Cosmopolitan. Ae. Albopictus: South-East Asia. Ae. Mediovittatus: Caribbean. Ae. Polynesiensis: Western Pacific Region. Distinct Physical Features Habitats: Tropical/Sub-tropical. Male feeds on plant nectar Female needs a blood protein to synthesize eggs. (Human, Animals, Birds, Monkeys). Life Span: 14-21 days. Lays 300 eggs during her life span Close-up of an Aedes mosquito
- 6. Transmission Cycles ForestForest species of Aedes Rural Peri-domestic Urban Domesticated Agypti + Albopictus Mosquito Feeding Habits
- 7. Worldwide distribution of Aedes aegypti , dengue virus serotypes, and dengue epidemic activity. Figure is modified from Gubler
- 8. Immunology and Pathogenesisof Dengue Pathogenesis: Two Theories [Immunological & Virological theories]. Replication in a number of cells: Macrophages, Monocytes , B cells, mast cells, Dendritic cells, Endothelial cells. Viral entry: Fc-gamma receptors of the host cells. Fc-gamma: Implicated in ADE. The genetic determinants on E gene and the 5’ and 3’ untranslated regions (The viral Theory). Dengue virus reactive T-cells: React differently with various serotypes. Multiplicity of Genetic determinants.
- 9. Pathogenesis of DengueHost genetic + Environmental + Viral factors Absence of an animal model of disease: Candidate genes Identification for Susceptibility and Resistance. Host Genetics: Variability at HLA I loci, Fc-gamma, Vit D receptor, promoter region of CD209 ---- Associated with distinct symptomatic phenotypes. Host Immune pressure: Disease outcome + Viral evolution [within individual (quasispecies), or at geographic scale]. Expression of special class I alleles: Associated with outcome.
- 10. The Non-ADE andADE Pathway: Electron micrographs of Macrophages
- 11. Immunology of DengueAntibody Dependant Enhancement [IgG not IgM]. DEN1 (X Individual) ------ Ab (Anti-DEN1): [Life long Immunity] Ag:Ab complex (No entry into macrophages) DEN 2/3/4 (X) ---- Activation of Immune system [Takes it for the primary infection] Higher genetic similarity [ Similar surface proteins ]: The Immune system is tricked. Ab:Ag complexes [ No inactivation of the Ag ] Macrophages are attracted and infected : Sever consequences, infection becomes more acute, body releases cytokines [makes endothelial tissue more permeable] ------ DHF and Fluid loss . Vaccination & Passive acquisition of Abs in childern would have the same consequences.
- 12. Control Strategies Controlof Immature stages: Vector control [Larviciding with insecticides, elimination of breeding sites] Only temephos, permethrin, Bti, and pyriproxyfen are approved by WHO for use in drinking-water. Pyriproxyfen: Effective, new formulations are effective for 6 months, 1 ppb. Decrease fertility in adults. Limitations: Prevents only eclosion, Larvae and Pupae are active. BTi Toxins: Bacillus thuringiensis var. israelensis (Bti) High larvicidal activity in mosquitoes. Limitations: Combinations: BTi + Insecticide, BTi + Copepods: Effective but needs persistent follow up and supplementary food is needed. Others: Insecticide treated materials, Lethal ovitraps at airports.
- 13. Control Strategies BiologicalControl Strategies: Mosquito Densonucleosis viruses: Parvoviridae . 5 strains of Aedes DNVs. Direct lethal effect or shorten the life span of the mosquitoes. Limitation: Viral strains + Geographical location of vector = Variable outcome. Predatory copepods: Mesocyclops spp. (Crustacea; Eudecapoda). Control larvae. Limitations: Effective in some regions but are lost when there is no water. Monitoring and management is difficult.
- 14. Control Strategies GeneticModification of the Mosquitoes: Using Wolbachia. Stable Transformation of mosquitoes. Raising mosquitoes in lab. Collect the ova --------- microinjections of wolbachia into the germ line cells before cellularization. Collect the surviving larvae and raise them in separate vials containing fly medium. Cross the infected mosquitoes with wild type. Test the progeny for the presence of wolbachia by PCR using wolbachia-specific primers. Do more crosses to multiply the number. Release into the wild.
- 15. Control Strategies Mechanismof the cross: Transformation of the Mosquito Population Female Infected [ Wol+ ] X Male [Wild type] = Infected M/F. Female [ Wild type ] X Male [ Infected Wol+ ] = Sterile Eggs.
- 16. Some Concerns Ourfocus: Fumigations, Use of Insecticides, Strengthening Treatment and Diagnostics. Limitations of the focused areas: Economic concerns. Environmental concerns. Our social scenario and the existing operations. Transportations. Re-emergence? Cuba (1981-95).
- 17. Research Areas Transformationof the mosquito population. Molecular Epidemiological Studies. Association studies. Comparative genomics and sequencing. Immunology of the prevalent viral strains. DHF/DSS: May well occur without pre-existing antibodies..? New models of diseases. New targets? Novel vector search. Effective Predators.
- 18.