Association of dengue virus infection susceptibility with polymorphisms of 2′-5′-oligoadenylate synthetase genes: a case–control study

Thamizhmani, Ramanathan; Vijayachari, P.

doi:10.1016/j.bjid.2014.03.004

Cited by 25 publications

(18 citation statements)

References 15 publications

(16 reference statements)

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“…The implication of this protein in the control of DENV infection has been demonstrated in vitro and in rhesus macaques (Warke and others 2003;Sariol and others 2007). In addition, polymorphisms in the OAS1, OAS3, and OAS2 genes are associated with differential susceptibility to clinical outcomes of dengue infection (Alagarasu and others 2013;Thamizhmani and Vijayachari 2014). Taken together, these results show that both PKR and OAS, which are produced upon IFN-I stimulation, inhibit the viral replication cycle by inhibiting either DENV RNA translation or RNA degradation…”

Section: Ifn-i Response In Viral Infectionsmentioning

confidence: 89%

Dengue Virus Control of Type I IFN Responses: A History of Manipulation and Control

Ramı́rez

Urcuqui-Inchima

2015

Journal of Interferon & Cytokine Research

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The arthropod-borne diseases caused by dengue virus (DENV) are a major and emerging problem of public health worldwide. Infection with DENV causes a series of clinical manifestations ranging from mild flu syndrome to severe diseases that include hemorrhage and shock. It has been demonstrated that the innate immune response plays a key role in DENV pathogenesis. However, in recent years, it was shown that DENV evades the innate immune response by blocking type I interferon (IFN-I). It has been demonstrated that DENV can inhibit both the production and the signaling of IFN-I. The viral proteins, NS2A and NS3, inhibit IFN-I production by degrading cellular signaling molecules. In addition, the viral proteins, NS2A, NS4A, NS4B, and NS5, can inhibit IFN-I signaling by blocking the phosphorylation of the STAT1 and STAT2 molecules. Finally, NS5 mediates the degradation of STAT2 using the proteasome machinery. In this study, we briefly review the most recent insights regarding the IFN-I response to DENV infection and its implication for pathogenesis.

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Section: Ifn-i Response In Viral Infectionsmentioning

confidence: 89%

Dengue Virus Control of Type I IFN Responses: A History of Manipulation and Control

Ramı́rez

Urcuqui-Inchima

2015

Journal of Interferon & Cytokine Research

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“…Haralambieva with colleagues (2010) demonstrated that minor alleles of SNPs rs1732778 and rs2464288 located within the OAS2 gene are related to the higher level of specific antibodies upon rubella immunization. SNP rs1732778 is associated with sensibility to the flaviviral diseases: TBE and Dengue fever (Alagarasu et al, 2013;Thamizhmani, Vijayachari, 2014). It should be pointed that SNP rs1732778 is located at a distance of 7397 bp from the 3 ′ -region of the OAS2 gene (UCSC Genome Browser Gateway, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…In groups with severe TBE cases (central nervous system damages as meningo-encephalitic form of the disease) and milder ones without central nervous system damages (meningeal form, fever) and/or population control, analysis of 23 SNPs within OAS1, OAS2, OAS3 and OASL genes has previously revealed statistically significant distinction between genotype, allele and/or haplotype frequencies by five SNPs; those were rs1293762 (intron2), rs15895 (3 ′ -UTR), rs1732778 (3'-flanking region) of OAS2 genes and rs2285932 (exon6, Ile438Ile), rs2072136 (exon8, Ser567Ser) of OAS3 genes . SNPs within the genes of OAS family are associated with susceptibility to other diseases caused by flaviviruses, such as West Nile fever (Yakub et al, 2005;Lim et al, 2009;Bigham et al, 2011;Danial-Farran et al, 2015) and Dengue fever (Alagarasu et al, 2013;Thamizhmani, Vijayachari, 2014) Ассоциация генов OAS c иммунитетом против клещевого энцефалита of 23 SNPs in the OAS cluster with the level of antibodies and interleukin-4, interleukin-6 and interleukin-10 secretion upon rubella vaccination. The study targets to determine possible association between SNPs located within OAS2 and OAS3 genes being previously associated with the development of severe forms of TBE, and the formation of antibodies and cytokines upon vaccination against TBE.…”

mentioning

confidence: 99%

Association Between Polymorphisms in Genes Encoding 2′-5′-Oligoadenylate Synthetases and the Humoral Immune Response Upon Vaccination Against Tick-Borne Encephalitis

Yudin¹,

Igoshin²,

Lutova³

et al. 2018

Vestn. VOGiS

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Vaccination forms active immunity and represents an effective way of preventing tick-borne encephalitis (TBE). However, excessive vaccination is unjustified in terms of economics and medical ethics. One of the individualized approaches to vaccines is the selection of vaccine doses depending on the expected levels of immune response. Therefore, there is a need for new methods for assessing potential human immune responses prior to vaccination. The aim of this study was to determine possible association between single nucleotide polymorphisms (SNPs) located within OAS2 and OAS3 genes, which have been previously associated with the development of severe forms of TBE, and the formation of antibodies and cytokines upon vaccination against TBE. The study involved 97 volunteers of both sexes who had not previously been vaccinated against TBE and had no contact with ticks. Venous blood samples were collected one month after vaccination against TBE using the EnceVir vaccine. Levels of specific IgG antibodies against tick-borne encephalitis virus and interleukin 4 (IL-4) were analyzed. Genomic DNA samples were genotyped for the SNPs rs2285932, rs2072136, rs1293762, rs15895 and rs1732778 in genes encoding 2’-5’-oligoadenylate synthetases OAS2 and OAS3. Antibody production in response to vaccine administration was significantly associated with SNP rs1732778 in the regulatory region of the OAS2 gene. This indicator was significantly higher in people with heterozygous genotypes G/A as compared to people with homozygous genotypes G/G and A/A. Carriers of the A allele (G/A or A/A genotypes) of the same SNP had reduced IL-4 levels as compared to the homozygous G/G individuals. Thus, the data obtained indicate that SNP rs1732778 in the regulatory region of the OAS2 gene correlates with the formation of antiviral IgG antibodies and changes in IL-4 levels upon vaccination. Evidently, the genetic polymorphism in OAS2 gene should be considered when performing individualized TBE vaccinations.

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“…As mentioned above, polymorphisms at Oas1b have been shown to drive resistance to flaviviral infections in mice ( 37 , 40 ). Furthermore, genetic variation in OAS family members, such as Oas1 , the putative human homologue to Oas1b , have been shown to influence WNV disease ( 41 ), as well as dengue ( 42 ) and hepatitis C virus ( 39 ) in humans. However, despite the dominant role of Oas1/Oas1b in these populations in driving overall symptoms/susceptibility to WNV, there remains a range of pathogenic differences in both the human population as well as in our CC RIX lines, even among CC RIX group with identical Oas1b allele classifications.…”

Section: Discussionmentioning

confidence: 99%

Genetic Diversity in the Collaborative Cross Model Recapitulates Human West Nile Virus Disease Outcomes

Graham

Thomas

Swarts

et al. 2015

mBio

112

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West Nile virus (WNV) is an emerging neuroinvasive flavivirus that now causes significant morbidity and mortality worldwide. The innate and adaptive immune responses to WNV infection have been well studied in C57BL/6J inbred mice, but this model lacks the variations in susceptibility, immunity, and outcome to WNV infection that are observed in humans, thus limiting its usefulness to understand the mechanisms of WNV infection and immunity dynamics. To build a model of WNV infection that captures human infection outcomes, we have used the Collaborative Cross (CC) mouse model. We show that this model, which recapitulates the genetic diversity of the human population, demonstrates diversity in susceptibility and outcomes of WNV infection observed in humans. Using multiple F1 crosses of CC mice, we identified a wide range of susceptibilities to infection, as demonstrated through differences in survival, clinical disease score, viral titer, and innate and adaptive immune responses in both peripheral tissues and the central nervous system. Additionally, we examined the Oas1b alleles in the CC mice and confirmed the previous finding that Oas1b plays a role in susceptibility to WNV; however, even within a given Oas1b allele status, we identified a wide range of strain-specific WNV-associated phenotypes. These results confirmed that the CC model is effective for identifying a repertoire of host genes involved in WNV resistance and susceptibility. The CC effectively models a wide range of WNV clinical, virologic, and immune phenotypes, thus overcoming the limitations of the traditional C57BL/6J model, allowing genetic and mechanistic studies of WNV infection and immunity in differently susceptible populations.

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Association of dengue virus infection susceptibility with polymorphisms of 2′-5′-oligoadenylate synthetase genes: a case–control study

Cited by 25 publications

References 15 publications

Dengue Virus Control of Type I IFN Responses: A History of Manipulation and Control

Dengue Virus Control of Type I IFN Responses: A History of Manipulation and Control

Association Between Polymorphisms in Genes Encoding 2′-5′-Oligoadenylate Synthetases and the Humoral Immune Response Upon Vaccination Against Tick-Borne Encephalitis

Genetic Diversity in the Collaborative Cross Model Recapitulates Human West Nile Virus Disease Outcomes

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