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

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mean DENV titers 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  by the presence of dsRNA in an infected cell. 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 using RNAi to modulate DENV replication, DENV infection can activate Toll pathways in response to dsRNA [25]. The presence of bacterial flora in the gut of mosquitoes also influences the  Toll pathway response and has an overlapping immune response that affect dengue virus replication by increasing the levels of different microbial proteins within the infected cell. In figure ? the DENV titers in the midgut of infected mosquitoes raised in a microbe free enviroment (aseptic) are much higher than mosquitoes raised septically [25].
 
mean DENV titers 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  by the presence of dsRNA in an infected cell. 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 using RNAi to modulate DENV replication, DENV infection can activate Toll pathways in response to dsRNA [25]. The presence of bacterial flora in the gut of mosquitoes also influences the  Toll pathway response and has an overlapping immune response that affect dengue virus replication by increasing the levels of different microbial proteins within the infected cell. In figure ? the DENV titers in the midgut of infected mosquitoes raised in a microbe free enviroment (aseptic) are much higher than mosquitoes raised septically [25].
[[File:Septicvsaseptic.jpg‎|400px|thumb|left|Figure ?. Amount of virus (in plaque forming units) from the midguts of mosquitoes raised with (septic) or without microbial flora (aseptic).[25]]]
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[[File:Septicvsaseptic.JPG‎|400px|thumb|left|Figure ?. Amount of virus (in plaque forming units) from the midguts of mosquitoes raised with (septic) or without microbial flora (aseptic).[25]]]
  
 
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Revision as of 20:38, 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 DENV titers 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 by the presence of dsRNA in an infected cell. 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 using RNAi to modulate DENV replication, DENV infection can activate Toll pathways in response to dsRNA [25]. The presence of bacterial flora in the gut of mosquitoes also influences the Toll pathway response and has an overlapping immune response that affect dengue virus replication by increasing the levels of different microbial proteins within the infected cell. In figure ? the DENV titers in the midgut of infected mosquitoes raised in a microbe free enviroment (aseptic) are much higher than mosquitoes raised septically [25].

Figure ?. Amount of virus (in plaque forming units) from the midguts of mosquitoes raised with (septic) or without microbial flora (aseptic).[25]


To further complicate Aedes aegypti

Effects of Wolbachia on Dengue Replication and Transmission in Vector Host