Dengue hemorrhagic fever – A systemic literature review of current perspectives on pathogenesis, prevention and control

Wang, Wen‐Hung; Urbina, Aspiro Nayim; Chang, Max R.; Assavalapsakul, Wanchai; Lu, Po‐Liang; Chen, Yen-Hsu; Wang, Sheng-Fan

doi:10.1016/j.jmii.2020.03.007

Cited by 172 publications

(141 citation statements)

References 127 publications

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“…DHF Grades I and II are relatively moderate non-shock events, while shock events are more extreme and accompanied by grades III and IV [40]. Hypovolemic shock due to excessive plasma leakage may occur in some infected individuals [41]. The life-threatening DSS develops at or shortly after grade III fever reduction and is defined by a damp and clammy face with a weak pulse or hypotension.…”

Section: Dengue Hemorrhagic Fever and Dengue Shock Syndromementioning

confidence: 99%

“…Actually, in around 20 dengueendemic countries in Asia, Latin America, Oceania and Europe, there is only one vaccine approved for the protection against dengue. This LVA recombinant tetravalent vaccine is the Dengvaxia (CYD-TDV) established by Sanofi Pasteur [41]. Phase III experiments revealed the vaccine's effectiveness that relied on age, serostatus, and serotype and revealed a benefit at the population level.…”

Section: Live Attenuated Vaccines (Lav)mentioning

confidence: 99%

“…There is a need for a safe, reliable, and economical tetravalent dengue vaccine for global public health. One approved vaccine is Dengvaxia by Sanofiadministration of the vaccine has been widely debated by various parties [41].…”

Section: Future Prospectsmentioning

confidence: 99%

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Dengue Virus: Infection, Immunological Response, and Vaccine Development

Sindi

2021

JPRI

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In the tropics and subtropics climates worldwide, the dengue virus (DENV) is the most common of arboviruses and a significant public health threat. The severe disease usually occurs during the primary infection, but more serious cases begin after the second instance of infection with a different serotype. Humans' innate immune system is composed of monocytes, macrophages, and dendritic cells, and they are capable of mounting rapid inflammatory responses. These cells are also called primary antigen-presenting cells, and they are essential for the formation of the immune system's long-term memory mechanisms. Through scientific advances, valuable knowledge into the pathogenesis of more serious diseases, and new methods to the production of dengue vaccines and antiviral drugs have been provided. We summarized details in the current literature review, including references, abstracts, and full text of journal articles. So that, we tried to review all available studies that projected existing awareness about the immune response to the dengue virus and the current status of the vaccine. Such information was selected and extracted from the PubMed, Web of Science, and Google Scholar databases for published data from 2000 to 2020 using relevant keywords containing a combination of terms, including dengue fever, epidemiology, clinical manifestation, immune response, and vaccine.

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Section: Dengue Hemorrhagic Fever and Dengue Shock Syndromementioning

confidence: 99%

Section: Live Attenuated Vaccines (Lav)mentioning

confidence: 99%

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Dengue Virus: Infection, Immunological Response, and Vaccine Development

Sindi

2021

JPRI

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“…This Part II of the dengue immunopathogenesis section will address the multifactorial immunopathogenic process of DENV infection from the perspective of the pre-existing serotype cross-reactive antibodies, the hyperactivation of DENVinfected immune cells (e.g. monocytes, mast cells) leading to increased cytokine production, the role of T cell responses, the activation of complement pathways, and the new pathogenic roles of the secreted NS1 of DENV that may act together to occasionally cause severe dengue manifestations followed by shock and potentially death [1,[6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21].…”

Section: Dengue Immunopathogenesis and Severe Disease: Host And Viralmentioning

confidence: 99%

“…Plasma circulating levels of soluble NS1 (sNS1) have been described to correlate with the appearance of severe disease manifestations such as dengue hemorrhagic fever (DHF) in DENV-infected patients [15]. sNS1 from DENV has been shown to act as a potential pathogen associated-molecular pattern (PAMP) that on immune cells and platelets interacts with Toll-like receptor 4 (TLR4), a pattern-recognition-receptor (PPR) [16] resulting in the production of pro-inflammatory cytokines from human PBMCs and monocytes [17] and the activation of human platelets which results in their aggregation and increase adherent onto the ECs lining the blood vessels, which hampers the homeostasis of the EC-barrier and the microvasculature [18]. Due to its ability to trigger the production of cytokines via TLR4, the term 'viral toxin' is now used to describe this pathogenic function of sNS1 during systemic DENV infection [14].…”

Section: Antibody Response To Denv Infectionmentioning

confidence: 99%

Dengue Immunopathogenesis: A Crosstalk between Host and Viral Factors Leading to Disease: PART II - DENV Infection, Adaptive Immune Responses, and NS1 Pathogenesis

Puerta-Guardo¹,

Biering²,

Harris³

et al. 2020

Dengue Fever in a One Health Perspective

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Severe disease is associated with serial infection with DENV of different serotypes. Thus, primary DENV infections normally cause asymptomatic infections, and secondary heterotypic infections with a new DENV serotype potentially increase the risks of developing severe disease. Despite many proposed hypotheses trying to explain it, the exact immunological mechanism leading to severe dengue disease is unknown. In turn, severe manifestations are believed to be a consequence of the combinations of many immunopathogenic mechanisms involving viral and host factors leading to increased pathogenesis and disease. Of these mechanisms, the adaptive immune response has been proposed to play a critical role in the development of severe dengue manifestations. This includes the effect of non-neutralizing but enhancing antibodies produced during primary infections, which results in enhanced-DENV infection of Fc-γ-receptor-expressing cells (e.g. monocytes and macrophages) during DENV heterotypic exposure in a phenomenon called antibody-dependent enhancement (ADE); the increased activation of memory T cells during secondary infections, which has low affinity for the current infecting serotype and high affinity for a past infection with a different serotype known as the original antigenic sin; the unbalanced production of pro-inflammatory cytokines that have a direct effect on vascular endothelial cells resulting in plasma leak in a phenomenon known as cytokine storm; and the excessive activation of the complement system that causes exacerbated inflammatory responses, increasing disease severity. In addition to the adaptive immune responses, a secreted viral factor known as the nonstructural protein 1 (NS1) has been recently proposed as the missing corner piece of the DENV pathogenesis influencing disease. This Part II of the chapter will discuss the interplay between the distinct host adaptive immune responses and viral factors that together contribute to the development of DENV pathogenesis and severe disease.

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