Effects of Pathogen-Vector Interactions on the Transmission of Dengue Virus: Difference between revisions

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==Viral factors that affect DENV replication and transmission in the mosquito vector==
==Vector host-factors that affect DENV replication and transmission in the mosquito vector==
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The transmission from vector to host for a particular DENV strain is determined by viral infectivty of mosquito cells, and the rate of viral replication in these cells.
Some of the host factors that specifically influence dengue infection and transmission are <I>Aedes</I> innate immune system response to viral infection and vector immune response to co-infection of dengue virus and the parasitic bacterium <I>wolbachia</I> [4,6,13].  
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[[File:Percent of headsinfected versus mean virus titer.jpg‎|400px|thumb|right|Figure ?. positive correlation between percent of heads infected (arcsin-square root transformation)and the mean body virus titer in mosquitoes infected with DENV-3 strains.[4]]]
==Innate Immune Response of Vector==
Dissemination from the heomocoel to the salivary glands affects disease transmission as well but it is tied directly tied to viral replication rates and viral titers in the hemocoel as seen in figure ?[4].
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Replication rate and viral titers are both linked to genotypic differences between DENV strains. Strains belonging to more virulent genotypes have fast rates of viral replication as well as higher virus titers in human and vector hosts[4,23].
mean virus titer in mosquitoes can be modulated by blocking the function of one or more components in the RNA interference (RNAi) pathway. This innate immune response is triggered in an infected cell by the presence of dsRNA. In the case of DENV infection the secondary structure of the NTR of the RNA genome may trigger this response. The hairpin loops as seen in figure (the structure one) look like dsRNA[24]. Activation of the RNAi pathway leads to the degradation of dsRNA within the infected cell and although it does not completely inhibit infection, virus titers are lower in mosquito cells with a functional RNAi response as opposed to mosquito cells without a functional response [24].
[[File:Viral output DCs.jpg‎|400px|thumb|right|Figure ?.Southeast Asian genotype strains had higher viral titers than American genotype strains in human donor dendritic cells 48 hours post-infection.[23]]]
[[File:Viral titer between DENV 3 innassive and noninvassive.png‎|400px|thumb|right|Figure ?.Invasive DENV-3 strains had higher viral titers in infected mosquitoes than noninvasive strains.[4]]]
Figure ? shows greater viral output (defined as number of viral genomes over the number of infected cells) in donor dendritic cells 48 hours post-infection. Black bars represent data pooled from tweleve different Southeast Asian genotype strains, white bars represent data pooled from seven different American strains. In figure ? it is clear that the Invassive DENV-3 strains had higher viral titers than noninvassive strains.
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Differences in the encoded secondary structure nontranslated regions of the RNA genome (NTRs) are correlated with differences in virulence between strains. No specific nucleotide or amino acid differences in either the coding or noncoding region have been correlated with attenuated disease in humans. It is only clear that there are differences at these sights between more virulent strains and less virulent strains (figure ?). differences in the three dimmensional structure of the viral genome may affect the initation of translation. This could explain why more virulent strains have higher rates of replication.
Besides RNAi, mosquitoes
[[File:predicted2ndarystructures.jpg‎|400px|thumb|right|Figure ?. Predicted secondary RNA structures of the 3’ NTR of; a, an American genotype DENV-2 strain and b, a Southeast Asian DENV-2 strain.[23]]]
==Effects of <I>Wolbachia</I> on Dengue Replication and Transmission in Vector Host==
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Mutations in the sequence with in the envelope glycoprotein E have also been correlated with virulence but as of yet there are no specifc changes in nucloetide sequnce correlated with virulence [23].
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Revision as of 20:08, 7 December 2010


Vector host-factors that affect DENV replication and transmission in the mosquito vector


Some of the host factors that specifically influence dengue infection and transmission are Aedes innate immune system response to viral infection and vector immune response to co-infection of dengue virus and the parasitic bacterium wolbachia [4,6,13].

Innate Immune Response of Vector


mean virus titer in mosquitoes can be modulated by blocking the function of one or more components in the RNA interference (RNAi) pathway. This innate immune response is triggered in an infected cell by the presence of dsRNA. In the case of DENV infection the secondary structure of the NTR of the RNA genome may trigger this response. The hairpin loops as seen in figure (the structure one) look like dsRNA[24]. Activation of the RNAi pathway leads to the degradation of dsRNA within the infected cell and although it does not completely inhibit infection, virus titers are lower in mosquito cells with a functional RNAi response as opposed to mosquito cells without a functional response [24].

Besides RNAi, mosquitoes

Effects of Wolbachia on Dengue Replication and Transmission in Vector Host