TNF‐α‐308A allele, a possible severity risk factor of hemorrhagic manifestation in dengue fever patients

Fernández‐Mestre, Mercedes; Gendzekhadze, Ketevan; Rivas-Vetencourt, Pedro; Layrisse, Z.

doi:10.1111/j.1399-0039.2004.00304.x

Cited by 134 publications

(90 citation statements)

References 18 publications

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“…Fernandez-Mestre et al [12], when studying the SNPs TNF -308 G>A, TGFB1 The frequency of the genotype IL6 -174 GC in the patients with DF presented by the authors was similar to the one found in our study (26.8% vs. 27.9%). However, the frequency of this genotype in controls was significantly lower than ours (21.7% vs 38.3% personal communication), possibly because of a difference in the racial components formation of the two populations.…”

Section: Discussionsupporting

confidence: 76%

“…Recent studies show that immune response variations from polymorphisms *Address correspondence to this author at the Immunogenetics Lab, Clinical Analysis Department, Maringá State University, Maringá, Paraná, Brazil; E-mail: ramoliterno@uem.br and ramoliterno11@yahoo.com.br in regulatory regions of cytokine genes seem to influence the produced cytokine level and consequently the outbreak of different infectious disease, including Dengue Hemorrhagic Fever [10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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The Possible Protective Role of the Il6-174GC Genotype in Dengue Fever

Moreira¹,

Cardoso²,

Visentainer³

et al. 2008

TOTMJ

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Dengue is the most important viral disease transmitted by arthropod vectors. At present, it is known four types of virus serotypes, DEN 1, 2, 3 and 4. Differences in the host susceptibility to infection as well as the severity of disease can not be due only to viral virulence. Variations in immune response as a consequence of polymorphisms in regulatory regions of cytokine genes may have influence on the disease outcome. The aim of this study was to verify the occurrence of associations between cytokine gene polymorphisms and Dengue Fever.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

The Possible Protective Role of the Il6-174GC Genotype in Dengue Fever

Moreira¹,

Cardoso²,

Visentainer³

et al. 2008

TOTMJ

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“…Host factors that increase the risk of severe dengue disease include female sex, several human leukocyte antigen (HLA) class I alleles, a promoter variant of the DC-SIGN receptor gene, a single-nucleotide polymorphism in the tumour necrosis factor (TNF) gene and AB blood group [31][32][33][34][35][36] . Host factors that reduce the risk of severe disease during a second dengue infection include race, second or third degree malnutrition, and polymorphisms in the Fcγ receptor and vitamin D receptor genes [37][38][39][40][41][42] .…”

Section: Dengue Virus Pathogenesismentioning

confidence: 99%

Dengue: a continuing global threat

et al. 2010

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Dengue fever and dengue haemorrhagic fever are important arthropod-borne viral diseases. Each year, there are ~50 million dengue infections and ~500,000 individuals are hospitalized with dengue haemorrhagic fever, mainly in Southeast Asia, the Pacific and the Americas. Illness is produced by any of the four dengue virus serotypes. A global strategy aimed at increasing the capacity for surveillance and outbreak response, changing behaviours and reducing the disease burden using integrated vector management in conjunction with early and accurate diagnosis has been advocated. Antiviral drugs and vaccines that are currently under development could also make an important contribution to dengue control in the future.Dengue is the most important arthropod-borne viral infection of humans. Worldwide, an estimated 2.5 billion people are at risk of infection, approximately 975 million of whom live in urban areas in tropical and sub-tropical countries in Southeast Asia, the Pacific and the Americas 1 . Transmission also occurs in Africa and the Eastern Mediterranean, and rural Europe PMC Funders GroupAuthor Manuscript Nat Rev Microbiol. Author manuscript; available in PMC 2015 February 19. Published in final edited form as:Nat Rev Microbiol. 2010 December ; 8(12 0): S7-16. doi:10.1038/nrmicro2460. Europe PMC Funders Author ManuscriptsEurope PMC Funders Author Manuscripts communities are increasingly being affected. It is estimated that more than 50 million infections occur each year, including 500,000 hospitalizations for dengue haemorrhagic fever, mainly among children, with the case fatality rate exceeding 5% in some areas [1][2][3][4] . The geographical areas in which dengue transmission occurs have expanded in recent years (FIG. 1), and all four dengue virus serotypes (DENV-1-4) are now circulating in Asia, Africa and the Americas, a dramatically different scenario from that which prevailed 20 or 30 years ago (FIG. 2). The molecular epidemiology of these serotypes has been studied in an attempt to understand their evolutionary relationships 11 .This Review will provide an update on our understanding of the pathogenesis of this successful pathogen, how we diagnose and control infection and the progress that has been made in vaccine development. Dengue virus pathogenesisDengue viruses belong to the genus flavivirus within the Flaviviridae family. DENV-1-4 evolved in non-human primates from a common ancestor and each entered the urban cycle independently an estimated 500-1,000 years ago 12 . The virion comprises a spherical particle, 40-50 nm in diameter, with a lipopolysaccharide envelope. The positive singlestrand RNA genome (FIG. 3), which is approximately 11 kb in length, has a single open reading frame that encodes three structural proteins -the capsid (C), membrane (M) and envelope (E) glycoproteins -and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5 [18][19][20] . ADE occurs when mononuclear phagocytes are infected through their Fc receptors by immune complexes that form between DE...

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“…4). The ability of DV-immune In addition to high levels of viremia, cytokine cascades are thought to contribute to severe dengue disease (8,13,42). Induction of cytokine signaling was recently reported in postentry events of DV infection under ADE conditions in monocytic cell lines (7,33).…”

Section: Discussionmentioning

confidence: 99%

Role of Dendritic Cells in Antibody-Dependent Enhancement of Dengue Virus Infection

Boonnak

Slike

Burgess

et al. 2008

J Virol

171

172

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Dengue viruses (DV), composed of four distinct serotypes (DV1 to DV4), cause 50 to 100 million infections annually. Durable homotypic immunity follows infection but may predispose to severe subsequent heterotypic infections, a risk conferred in part by the immune response itself. Antibody-dependent enhancement (ADE), a process best described in vitro, is epidemiologically linked to complicated DV infections, especially in Southeast Asia. Here we report for the first time the ADE phenomenon in primary human dendritic cells (DC), early targets of DV infection, and human cell lines bearing Fc receptors. We show that ADE is inversely correlated with surface expression of DC-SIGN (DC-specific intercellular adhesion molecule-3-grabbing nonintegrin) and requires Fc gamma receptor IIa (Fc␥RIIa). Mature DC exhibited ADE, whereas immature DC, expressing higher levels of DC-SIGN and similar Fc␥RIIa levels, did not undergo ADE. ADE results in increased intracellular de novo DV protein synthesis, increased viral RNA production and release, and increased infectivity of the supernatants in mature DC. Interestingly, tumor necrosis factor alpha and interleukin-6 (IL-6), but not IL-10 and gamma interferon, were released in the presence of dengue patient sera but generally only at enhancement titers, suggesting a signaling component of ADE. Fc␥RIIa inhibition with monoclonal antibodies abrogated ADE and associated downstream consequences. DV versatility in entry routes (Fc␥RIIa or DC-SIGN) in mature DC broadens target options and suggests additional ways for DC to contribute to the pathogenesis of severe DV infection. Studying the cellular targets of DV infection and their susceptibility to ADE will aid our understanding of complex disease and contribute to the field of vaccine development.

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TNF‐α‐308A allele, a possible severity risk factor of hemorrhagic manifestation in dengue fever patients

Cited by 134 publications

References 18 publications

The Possible Protective Role of the Il6-174GC Genotype in Dengue Fever

The Possible Protective Role of the Il6-174GC Genotype in Dengue Fever

Dengue: a continuing global threat

Role of Dendritic Cells in Antibody-Dependent Enhancement of Dengue Virus Infection

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