Dengue virus (DENV) is a mosquito-transmitted RNA virus that infects an estimated million humans each year. Here, we review recent advances in our  ‎Dengue virus epidemiology · ‎DENV pathogenesis · ‎Dengue virus biology. Dengue is the most common and important arthropod-borne viral (arboviral) illness in humans. It is transmitted by mosquitoes of the genus. NS1 antigen in dengue virus has been shown to regulate complement activation and hence could play a role in the pathogenesis of DHF [


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Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

Similarly, DENV infection patterns in microvascular cells in vitro suggest that EC from different tissues have different activation patterns In this regard, it is worth mentioning that the major nonstructural dengue virus pathogenesis 1 NS1 of DENV has been dengue virus pathogenesis to bind preferentially to EC of lung and liver tissues 9.

It has been hypothesized that recognition of NS1 by anti-NS1 antibodies could then contribute to the selective pulmonary vascular leakage. Virus Virulence According to the virus virulence hypothesis, certain DENV strains are responsible for more severe disease.

DENV serotypes can be further classified into different genotypes on the basis of nucleotide variations.

Dengue fever - Wikipedia

Viral genetic differences have been associated with differences in virulence 51, Remarkably, the first outbreak of DHF in the Americas occurred inwhich coincided with the introduction of the possibly more virulent DENV-2 Southeast Asian genotype, while the less virulent indigenous DENV-2 genotype was already circulating in the region- It has also been proposed that intraepidemic evolution of the circulating DENV might be responsible for increased severity of disease.

During the DENV-2 epidemic in Cuba, it was noted that severity of disease manifestations and case-fatality rates were increased toward the end dengue virus pathogenesis the epidemic, suggesting that the circulating DENV-2 might have become more virulent through passage in hosts during the epidemic.

A similar situation was observed in the Dengue virus pathogenesis epidemic in Townsville, Australiaand again in Cuba during the epidemic Analysis of DENV genomes has shown that DENV indeed evolves during an epidemic 42; however, more data are needed to establish an association between intraepidemic virus evolution and increased disease severity.

Epidemiological observations in the Americas and in Singapore suggested that the sequence of infection with particular serotypes and the time interval between primary infection and secondary infection may play an important role in the development of DHF. Furthermore, these studies indicated that the longer the interval between primary and secondary infections, the higher the risk of developing severe disease.


In addition, age has been shown to influence the outcome of disease following a secondary infection with heterologous DENV In Asia, the risk of severe disease is greater in children than in adults, in contrast to the Americas, where the adult population is mainly affected and infection results in milder dengue virus pathogenesis.

This difference in disease severity caused by Asian and American genotypes correlated with structural differences in the two strains of DENV 51 Dengue virus pathogenesis has also been shown that different geographical DENV strains or different serotypes may vary in their ability to infect different cell types or cause severe disease 56 It is important to realize that virulence has traditionally been considered a microbial property, evaluated independently of the host or only in vitro or in often inbred animals.

However, an increasing body of evidence incriminates the host immune response in the pathogenesis of many microbial infections Therefore, in studying DENV virulence, both host and viral factors should be considered.

Activation of the Complement System The complement system is one of the main humoral components of the innate immunity and interacts closely with the hemostatic system to provide the first line of defense against pathogens.

These innate immune mechanisms provide the host with the time needed to maximally induce the more slowly developing adaptive immunity. With regard to DENV, investigators noticed that around the time of defervescence, when plasma leakage may become apparent, high dengue virus pathogenesis of the activation products C3a and C5a are measured in the plasma, followed by an accelerated consumption dengue virus pathogenesis a marked reduction of the complement components in patients with DSS 50, Therefore, it was hypothesized that complement activation plays an important role in the pathogenesis of dengue.

However, many aspects of complement activation and its role in DENV pathogenesis remain to be investigated.

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  • Dengue Virus Pathogenesis: an Integrated View

It has been proposed that NS1 is an important trigger for complement activation Binding of heterotypic antibodies to NS1 expressed on infected cells may result in complement activation 8 In addition, it is believed that NS1 released from infected cells can dengue virus pathogenesis activate complement factors present in the fluid phase Alternatively, the C5b-C9 complex could independently trigger other local and systemic effectswhich may be implicated in intravascular coagulation.

It is important to realize that coagulation enzymes can also activate the complement system, illustrating the extensive interaction that exists between the complement and the coagulation system. Several groups have shown that both IgG1 and IgG3 were the predominant subclasses involved in the specific antibody response in dengue virus pathogenesis DENV infections As a result, less blood circulates in the blood vessels, and the blood pressure becomes so low that it cannot supply sufficient blood to vital organs.

Dengue virus pathogenesis, dysfunction of the bone marrow due to infection of the stromal cells leads to reduced numbers of platelets, which are necessary for effective blood clotting; this increases the risk of bleeding, the other major complication of dengue fever.

Meanwhile, the virus genome is translated in membrane-bound vesicles on the cell's endoplasmic reticulumwhere the cell's protein synthesis apparatus produces new viral proteins that replicate dengue virus pathogenesis viral RNA and begin to form viral particles.

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