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

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==Transmission Cycle==
==Viral factors that affect DENV replication and transmission in the mosquito vector==
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The transmission of a particular strain of dengue from vector to host is determined by how infective the virus is in the vector, the level of viral replication in tissues of the vector, and how easily the virus can disseminate from the midgut to the salivary glands [4]. Infectivity, replication, and dissemination are affected by both the genotype of the infecting virus as well as a variety of mosquito host factors that modulate dengue virus infection.
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More virulent strains have fast rates of viral replication as well as higher virus titers in both human host and vector host. It seems as though mutations within the E envelope glycoprotein responsible for virion binding to the host cell receptor increases the infectivity of a strain. Differences in the nontranslated regions of the genome (NTRs) also seem to affect virulence because possible changes in the time it takes to initiate translation because of changes in secondary structure as seen in figure (dengue virus structural… leitmeyer). 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.
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[[File: Skeeter-human-skeeter-human.gif‎|400px|thumb|left|Figure 4. Transmission cycle of dengue virus between human hosts and mosquito vectors.[10]]]
[[File:predicted2ndarystructures.jpg‎|400px|thumb|right|Figure ?. a predicted RNA secondary structure of the 3’ NTR of a strain representing a less virulent American genotype strain, b a more virulent southeast Asian genotype [15]]]
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The DENV transmission cycle begins when an infected mosquito bites a human or nonhuman primate host. The Host begins to experience symptoms four to seven days post-infection with symptoms usually lasting three to ten days after which there is about a three week recovery period [8]. The virus initially replicates in target organs like the liver, spleen, and thymus but eventually makes its way to the lymphatic system where it replicates in lymph tissue and white blood cells. The lymphatic system serves as a gateway to the bloodstream where the virus continues to replicate and can potentially infect the endothelial cells of the circulatory vasculature. Eventually virus titers are high enough in the host blood for disease transmission to occur. For a period of about five days, just before symptoms appear, the virus is transmissible to a new mosquito vector through an infected blood meal.
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After being taken up in an infected blood meal by a mosquito DENV replicates in the midgut of the insect and infects its hemocoel (body cavity). From the hemocoel, the virus eventually infects the salivary glands. Once virus titers are high enough in the salivary glands the mosquito can infect a new susceptible host when it goes for another blood meal [4]. The length of time required for virus to reach the salivary glands of a mosquito after the ingestion of an infected blood meal is about eight to ten days depending on both viral and host factors [8]. The delay between ingestion of an infected blood meal and infection and replication of DENV in the salivary glands influences the course of epidemics and plays a role in competition between DENV strains.

Revision as of 18:23, 7 December 2010


Viral factors that affect DENV replication and transmission in the mosquito vector



The transmission of a particular strain of dengue from vector to host is determined by how infective the virus is in the vector, the level of viral replication in tissues of the vector, and how easily the virus can disseminate from the midgut to the salivary glands [4]. Infectivity, replication, and dissemination are affected by both the genotype of the infecting virus as well as a variety of mosquito host factors that modulate dengue virus infection.

More virulent strains have fast rates of viral replication as well as higher virus titers in both human host and vector host. It seems as though mutations within the E envelope glycoprotein responsible for virion binding to the host cell receptor increases the infectivity of a strain. Differences in the nontranslated regions of the genome (NTRs) also seem to affect virulence because possible changes in the time it takes to initiate translation because of changes in secondary structure as seen in figure (dengue virus structural… leitmeyer). 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 ?. a predicted RNA secondary structure of the 3’ NTR of a strain representing a less virulent American genotype strain, b a more virulent southeast Asian genotype [15]


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