Pathogenesis of Dengue Haemorrhagic Fever: Current Perspectives

Pang, Tikki

doi:10.1007/978-1-4684-5712-4_15

Cited by 4 publications

(5 citation statements)

References 39 publications

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“…The raised levels of immunoreactive TNF␣ in grade II and grade III dengue-infected patients in our study strongly indicate activation of the TNF␣ system during dengue infection. However, the mechanisms underlying the sensitization of a host to TNF␣ are not fully understood, and such influences together with virulence of dengue virus strain could explain the outcome of dengue infection in each patient [Pang, 1987;Wallach et al, 1990]. In order to elucidate whether the antiviral effect or pathophysiological role of TNF␣ predominates in dengue infection, studies of the variations of TNF␣ and virus isolation in sequential blood samples obtained consecutively for several days in dengue-infected patients should be performed.…”

Section: Discussionmentioning

confidence: 98%

“…Although dengue virus infection (four serotypes in the flavivirus genus of the Flaviviridae family) usually results in mild disease, sometimes infection by this virus results in a severe disease such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) [Cohen and Halstead, 1966]. The pathogenesis of dengue is incompletely understood, but some evidence suggests that an abnormal immune response and a disturbance in immune regulation may be responsible for the pathogenesis of shock and excessive hemorrhage in patients with DHF/DSS [Halstead, 1989;Pang, 1987;Suvatte, 1987]. Cytokines are involved in immune regulation but could play a role in pathologic manifestations of dengue infection [Halstead, 1989].…”

Section: Introductionmentioning

confidence: 99%

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Tumor necrosis factor alpha levels in plasma and whole-blood culture in dengue-infected patients: Relationship between virus detection and pre-existing specific antibodies

Hober

Nguyen²,

Shen

et al. 1998

J. Med. Virol.

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The pathogenesis of dengue hemorrhagic fever (DHF) is not well known, but the role of host factors has been suggested. The level of immunoreactive circulating and cell-generated tumor necrosis factor alpha (TNF alpha) was studied in 35 patients with DHF; its relationship with virus isolation and/or genome detection by reverse transcription polymerase chain reaction (RT-PCR) and specific antibodies were detected by hemagglutination inhibition (HI). Large variation of TNF alpha plasma levels was obtained in dengue-infected patients at the same stage of the disease and at the same day after infection. Most of the patients (14 out of 17 patients) who displayed augmented spontaneous in vitro production of TNF alpha by heparinized whole-blood culture compared with controls also had elevated levels of TNF alpha in the plasma. The TNF alpha values in lipopolysaccharide and phytohemagglutinin heparinized whole-blood cultures were not higher in patients than in controls, but low TNF alpha levels were obtained in three out of 30 patients. An inverse correlation was observed between spontaneous in vitro TNF alpha production and viral replication, which raises the issue of the antiviral effect of TNF alpha in dengue infection. The results do not support the hypothesis of the role of antibody-dependent enhancement giving rise to increased viremic titers and production of TNF alpha in patients. The present study demonstrates the activation of the TNF alpha-producing cells in dengue-infected patients and suggests further investigation to define the mechanism and the role of TNF alpha in the pathogenesis of dengue virus infection.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor alpha levels in plasma and whole-blood culture in dengue-infected patients: Relationship between virus detection and pre-existing specific antibodies

Hober

Nguyen²,

Shen

et al. 1998

J. Med. Virol.

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“…However, the mechanisms by which these pathophysiological changes occur is incompletely understood. 7,8 Some evidence suggests an abnormal immune response and a disturbance in immune regulation as the basis of the pathogenesis. 9 The lack of pathological findings in major organs in most cases of fatal DHF/ DSS and rapid recovery of those who survive the critical period, suggest that physiologic dysfunction is secondary to the action of soluble mediators as these are capable of producing severe illness with minimal structural injury.…”

Section: Introductionmentioning

confidence: 99%

“…9 The lack of pathological findings in major organs in most cases of fatal DHF/ DSS and rapid recovery of those who survive the critical period, suggest that physiologic dysfunction is secondary to the action of soluble mediators as these are capable of producing severe illness with minimal structural injury. 8,10,11 Macrophages are an important target of dengue virus infection, 2,12 which are known to produce various cytokines upon stimulation. 13,14 In dengue virus infection, cytokines may be released either directly from virus-infected cells such as monocytes/macrophages or upon interactions of virus-infected cells with other immune cells such as activated T lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory mediators in dengue virus infection in children: interleukin-6 and its relation to C-reactive protein and secretory phospholipase A2.

Juffrie

Meer²,

Hack³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

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Abstract. To assess the potential role of interleukin-6 (IL-6) in the pathogenesis of dengue virus infection, levels of this cytokine were measured in children with dengue virus infection on admission to the hospital. As presumed surrogate markers of IL-6, C-reactive protein (CRP) and secretory phospholipase A2 (sPLA2) were measured. Three groups were studied: 33 apparently healthy children as negative controls, 11 children with bacterial infections as positive controls, and 186 children with serologically documented dengue virus infection. One-hundred and fifteen patients had dengue fever (DF) and 71 had dengue hemorrhagic fever (DHF). Compared with healthy controls, dengue shock syndrome (DSS) patients had significantly higher levels of IL-6 on admission (P Ͻ 0.05), comparable with those in positive controls. Dengue patients with shock had significantly higher levels of IL-6 than normotensive patients (P Ͻ 0.001) and higher levels of IL-6 were associated with a higher incidence of ascites. C-reactive protein concentrations in dengue patients and in healthy children were not different, but lower than in children with bacterial infections (P ϭ 0.008). Secretory phospholipase A2 levels were higher in dengue patients than in apparently healthy children (P Յ 0.05) and similar to those in children with bacterial infection. Dengue shock syndrome patients had significantly higher sPLA2 concentrations than normotensive patients (P ϭ 0.02). These data indicate that IL-6 and sPLA2 may have a pathogenetic role only in the most severe forms of dengue virus infection.

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“…Although dengue virus infection usually results in mild disease, sometimes infection by this virus can result in a severe disease such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) (8). The pathogenesis of dengue is incompletely understood but some evidence suggests that an abnormal immune response and a disturbance in immune regulation may be responsible for the pathogenesis of shock and excessive hemorrhage in patients with DHF/DSS (12, 24,27). Cytokines are involved in immune regulation and could play a role in the pathologic manifestations of dengue infection (12).…”

mentioning

confidence: 99%

High Levels of sTNFR p75 and TNFα in Dengue‐Infected Patients

Hober

Delannoy

Benyoucef

et al. 1996

Microbiology and Immunology

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Soluble forms of the two molecular species of the cell surface TNF receptors (sTNFR p55 and sTNFR p75) can reduce the activity of TNFα but they may also enhance its function by stabilizing the active TNFα oligomer. Considering the pathophysiological importance of sTNFR p75 for the regulation of the bioavailability of TNFα in the body, we determined the serum levels of sTNFR p75 and TNFα in 45 children and 28 adults with laboratory‐confirmed dengue infection by using immunoassays. The serum samples were obtained from day 1 to day 15 after the onset of the disease during the 1989–1990 outbreak of dengue‐3 in Tahiti, French Polynesia. The patients were clinically classified as having dengue hemorrhagic fever (DHF) and graded according to the criteria of the World Health Organization (WHO) into four grades from less severe (grade I) to severe (grade IV). The sera of both children and adult patients of all severity grades contained higher levels of sTNFR p75 than the sera of control subjects. Although high levels of TNFα were also detected in children and adults among grade I, II, III and IV patients, we found no correlation between sTNFR p75 and TNFα. We observed in adults a moderate elevation of sTNFR p75 and TNFα in sera compared with that observed in children. The raised levels of immunoreactive sTNFR p75 and TNFα in all clinical groups of dengue‐infected patients strongly indicate activation of the TNFα system during dengue infection. The balance between sTNFR p75 and TNFα may be altered in dengue infection. Further investigations are needed to understand the role of sTNFR p75 and TNFα in the pathogenesis of DHF and to improve the management of dengue infection.

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Pathogenesis of Dengue Haemorrhagic Fever: Current Perspectives

Cited by 4 publications

References 39 publications

Tumor necrosis factor alpha levels in plasma and whole-blood culture in dengue-infected patients: Relationship between virus detection and pre-existing specific antibodies

Tumor necrosis factor alpha levels in plasma and whole-blood culture in dengue-infected patients: Relationship between virus detection and pre-existing specific antibodies

Inflammatory mediators in dengue virus infection in children: interleukin-6 and its relation to C-reactive protein and secretory phospholipase A2.

High Levels of sTNFR p75 and TNFα in Dengue‐Infected Patients

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