Publications by authors named "Aida G Romaschenko"

The progression of infectious diseases depends on causative agents, the environment and the host's genetic susceptibility. To date, human genetic susceptibility to tick-borne encephalitis (TBE) virus-induced disease has not been sufficiently studied. We have combined whole-exome sequencing with a candidate gene approach to identify genes that are involved in the development of predisposition to TBE in a Russian population.

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Previously, we studied an association of two IL28B gene single nucleotide polymorphisms (SNPs) and three IL10 gene SNPs with predisposition to tick-borne encephalitis in a Russian population. In this study, a possible involvement of these SNPs in the development of predisposition to chronic hepatitis C (caused by structurally similar, related virus from the Flaviviridae family) was investigated in the same population. Only the IL10 promoter rs1800872 SNP was associated with predisposition to chronic hepatitis C.

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Article Synopsis
  • * Previous research linked certain SNPs in these genes to chronic hepatitis C, indicating a potential common mechanism for resistance against similar viruses.
  • * The analysis involved comparing SNP frequencies in 132 TBE patients with a control group of 221 individuals from Novosibirsk, finding that specific IL28B and IL10 SNPs are associated with a higher risk of developing TBE.
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Background: The craniometric specificity of the indigenous West Siberian human populations cannot be completely explained by the genetic interactions of the western and eastern Eurasian groups recorded in the archaeology of the area from the beginning of the 2nd millennium BC. Anthropologists have proposed another probable explanation: contribution to the genetic structure of West Siberian indigenous populations by ancient human groups, which separated from western and eastern Eurasian populations before the final formation of their phenotypic and genetic features and evolved independently in the region over a long period of time. This hypothesis remains untested.

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Chronic hepatitis C is a severe liver disease caused by positive-strand RNA virus. Previously, we reported an association between seven single nucleotide polymorphisms (SNPs) in four innate immunity genes (OAS2, OAS3, CD209, and TLR3) and human predisposition to tick-borne encephalitis, caused by a virus from the same Flaviviridae family, in a Russian population. Currently, genotype and allele frequencies for these SNPs were analyzed in 75 chronic hepatitis C patients and compared with the population control (269 Novosibirsk citizens).

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Article Synopsis
  • Tick-borne encephalitis (TBE) is a serious CNS disease caused by the tick-borne encephalitis virus (TBEV).
  • A study in Russia looked at the genetic factors that might make some people more susceptible to TBE, specifically two polymorphisms: a 32bp deletion in the CCR5 gene and a single nucleotide polymorphism (SNP) in the TLR3 gene.
  • The research found that those with the G allele of the TLR3 SNP were more common in TBE patients, particularly in those with severe cases, suggesting a genetic link to susceptibility in this population.
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Coronary artery inflammation is a critical process in the pathogenesis of myocardial infarction (MI). The chemokine CCL5/RANTES (regulated upon activation, normal T cells expressed and secreted) is expressed in advanced atherosclerotic lesions. Functional polymorphisms of the RANTES gene can, therefore, be involved in the pathogenesis of coronary artery disease.

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The 2'-5'-oligoadenylate synthetase (2'-5'-OAS) family members are interferon-induced antiviral proteins. Twenty-three single nucleotide polymorphisms located within the OAS1, OAS2, OAS3, and OASL genes were analyzed in 142 patients with Russian tick-borne encephalitis. Statistically significant differences in genotype, allele, and haplotype frequencies for 3 OAS2 single nucleotide polymorphisms (rs1293762, rs15895, and rs1732778) and 2 OAS3 single nucleotide polymorphisms (rs2285932 and rs2072136) were detected between patients with central nervous system disease and both those with fever and/or meningitis and the control group.

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Background: Macrophage migration inhibitory factor (MIF) is a cytokine implicated in early and advanced atherosclerosis. The aim of this study was to investigate whether polymorphism of MIF gene is associated with myocardial infarction (MI).

Methods: Single nucleotide polymorphism (SNP) in MIF gene (-173G/C, rs755622) was investigated in Czech (n=219) and Russian (n=240) MI patients and population control from the same geographical areas (Czech, n=137; Russian, n=174).

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RNA polymerase III promoter is located within the coding region in all eukaryotic tRNA genes, whereas in prokaryotic tRNA genes, the promoter is located upstream of the transcription initiation site. We analyzed the nucleotide sequence context of the A and B boxes of RNA polymerase III promoters from different unicellular eukaryotes, plants, and animals and the homologous sequences in the tRNA genes of prokaryotic species (Archaea, Eubacteria). The long and short sequence variants of the A box are nonrandomly distributed across different types of the eukaryotic tRNA genes.

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