A variant in the CD209 promoter is associated with severity of dengue disease

Sakuntabhai, Anavaj; Turbpaiboon, Chairat; Casadémont, Isabelle; Chuansumrit, Ampaiwan; Lowhnoo, Tassanee; Kajaste‐Rudnitski, Anna; Kalayanarooj, Siripen; Tangnararatchakit, Kanchana; Tangthawornchaikul, Nattaya; Vasanawathana, Sirijit; Chaiyaratana, Wathanee; Yenchitsomanus, Pa Thai; Suriyaphol, Prapat; Avirutnan, Panisadee; Chokephaibulkit, Kulkanya; Matsuda, Fumihiko; Yoksan, Sutee; Jacob, Yves; Lathrop, G.M.; Malasit, Prida; Desprès, Philippe; Julier, Cécile

doi:10.1038/ng1550

Cited by 268 publications

(270 citation statements)

References 29 publications

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“…This observation is consistent with what was described by others, who were not able to replicate an association of À336A with TB in a small Colombia cohort. 25 Since the À871 SNP is absent in sub-Saharan Africans, our negative finding can only exclude a causal effect of À336, but we cannot confute a role for the À871/À336 haplotype in non-Africans. The apparent conflict of our data with that of Barreiro et al 5 can be explained by genetic heterogeneity (with different populations having differences in gene variants affecting risk) and is in agreement with the finding that their effect was mainly confined to people of Eurasian descent.…”

Section: Discussionmentioning

confidence: 64%

DC-SIGN (CD209), pentraxin 3 and vitamin D receptor gene variants associate with pulmonary tuberculosis risk in West Africans

et al. 2007

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We investigated the role of DC-SIGN (CD209), long pentraxin 3 (PTX3) and vitamin D receptor (VDR) gene single nucleotide polymorphisms (SNPs) in susceptibility to pulmonary tuberculosis (TB) in 321 TB cases and 347 healthy controls from GuineaBissau. Five additional, functionally relevant SNPs within toll-like receptors (TLRs) 2, 4 and 9 were typed but found, when polymorphic, not to affect host vulnerability to pulmonary TB. We did not replicate an association between SNPs in the DC-SIGN promoter and TB. However, we found that two polymorphisms, one in DC-SIGN and one in VDR, were associated in a nonadditive model with disease risk when analyzed in combination with ethnicity (P ¼ 0.03 for DC-SIGN and P ¼ 0.003 for VDR). In addition, PTX3 haplotype frequencies significantly differed in cases compared to controls and a protective effect was found in association with a specific haplotype (OR 0.78, 95% CI 0.63-0.98). Our findings support previous data showing that VDR SNPs modulate the risk for TB in West Africans and suggest that variation within DC-SIGN and PTX3 also affect the disease outcome.

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Section: Discussionmentioning

confidence: 64%

DC-SIGN (CD209), pentraxin 3 and vitamin D receptor gene variants associate with pulmonary tuberculosis risk in West Africans

et al. 2007

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“…The G allele of the variant of the promoter region (DC-SIGN-336) was associated with protection against dengue fever, but not dengue haemorrhagic fever. 96 This finding suggests that different disease phenotypes may be partly related to the activity of CD209 and the degree of DC-SIGN expression. Another area of focus in determining susceptibility to dengue has been polymorphisms in human platelet antigens (HPA).…”

Section: Genetic Determinants Of Dengue Susceptibilitymentioning

confidence: 99%

The pathogenesis of dengue

Whitehorn

Simmons

2011

Vaccine

226

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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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A variant in the CD209 promoter is associated with severity of dengue disease

Cited by 268 publications

References 29 publications

DC-SIGN (CD209), pentraxin 3 and vitamin D receptor gene variants associate with pulmonary tuberculosis risk in West Africans

DC-SIGN (CD209), pentraxin 3 and vitamin D receptor gene variants associate with pulmonary tuberculosis risk in West Africans

The pathogenesis of dengue

Dengue: a continuing global threat

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