scholarly journals Genetic source tracking of human plague cases in Inner Mongolia-Beijing, 2019

2021 ◽  
Vol 15 (8) ◽  
pp. e0009558
Author(s):  
Jianyun Li ◽  
Yumeng Wang ◽  
Fang Liu ◽  
Xiaona Shen ◽  
Yiting Wang ◽  
...  
Keyword(s):  
Inner Mongolia ◽  
Meriones Unguiculatus ◽  
Source Tracking ◽  
Snp Analysis ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Genome Wide ◽  
Genetic Source ◽  
Inner Mongolia Autonomous Region ◽  
Relationship Of

On 12 November 2019, one couple from the Sonid Left Qi (County) in the Inner Mongolia Autonomous Region was diagnosed with pneumonic plague in Beijing. The wife acquired the infection from her husband. Thereafter, two bubonic plague cases were identified in Inner Mongolia on November 16th and 24th. In this study, genome-wide single nucleotide polymorphism (SNP) analysis was used to identify the phylogenetic relationship of Yersinia pestis strains isolated in Inner Mongolia. Strains isolated from reservoirs in 2018 and 2019 in Inner Mongolia, together with the strain isolated from Patient C, were further clustered into 2.MED3m, and two novel lineages (2.MED3q, 2.MED3r) in the 2.MED3 population. According to the analysis of PCR-based molecular subtyping methods, such as the MLVA 14 scheme and seven SNP allele sequencing, Patients A/B and D were classified as 2.MED3m. In addition, strains from rodents living near the patients’ residences were clustered into the same lineage as patients. Such observations indicated that human plague cases originated from local reservoirs. Corresponding phylogenetic analysis also indicated that rodent plague strains in different areas in Inner Mongolia belong to different epizootics rather than being caused by spreading from the same epizootic in Meriones unguiculatus in 2019.

Whole Genome Association Study in Acute Myeloid Leukemia with a Normal Karyotype, Using a Single-Nucleotide Polymorphism (SNP) Analysis.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4253-4253
Author(s):  
Yongjun Cha ◽  
Kwang-Sung Ahn ◽  
Juwon Park ◽  
Byung-Su Kim ◽  
Soo-Mee Bang ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Myeloid Leukemia ◽  
Normal Karyotype ◽  
Snp Analysis ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Genome Wide ◽  
A Genome ◽  
Significant Difference ◽  
Acute Myeloid

Abstract As a result of numerous genetic aberrations, acute myeloid leukemia (AML) present with very heterogeneous clinical features. Moreover, structural and numerical chromosome aberrations currently comprise the most important basis for predicting these heterogeneous outcomes. However, 30 to 50 percent of AML patients have cytogenetically normal karyotypes. Though submicroscopic genetic alterations (such as NPM1, CEBPA, MLL-PTD) are increasingly being used for clinical purposes, additional markers with prognostic or predictive value are still lacking in this group. In this study, we performed a genome-wide, single-nucleotide polymorphism (SNP) study in order to identify novel genomic regions of interest in normal karyotype AML. 54 untreated AML patients with normal karyotypes were analyzed with an Illumina infinium 317K SNP chip assay. SNP genotype call rate was 99.8 percent, resulting in a resolution of 1 SNP/Mb. In a genome-wide SNP analysis, 317 SNP loci, having a significant difference between AML and normal control, were found. In addition, about 300 loci were also identified, showing a significant difference between patients who achieved CR and those who did not. Some of these were found to be related with drug metabolism and MDR family. Also we used the SNP assay to screen a loss of heterozygosity (LOH), suggesting possible involvement of tumor suppressor genes. In summary, 38 LOH regions larger than 1Mb were observed in 23 cases (43%) among 54 AML patients having normal karyotypes. Most (55%) of them were copy-neutral events and the most frequently identified alterations were located at 3p, 8p, 13q and 22q. 11 (29%) out of 38 LOH regions had overlapping parts among them. Some LOHs were correlated with response to chemotherapy. Various genetic changes were discovered by use of an SNP-based chip array in normal karyotype AML patients. Moreover, some of these were related with CR acquisition and drug metabolism. These results can be used to differentiate normal karyotype AML and warrant further study.

scholarly journals Mimicry diversification in Papilio dardanus via a genomic inversion in the regulatory region of engrailed – invected

2020 ◽  
Vol 287 (1926) ◽  
pp. 20200443 ◽  
Author(s):  
Martijn J. T. N. Timmermans ◽  
Amrita Srivathsan ◽  
Steve Collins ◽  
Rudolf Meier ◽  
Alfried P. Vogler
Keyword(s):  
Draft Genome ◽  
Regulatory Region ◽  
Snp Analysis ◽  
The Novel ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Geographic Spread ◽  
Genome Wide ◽  
Wing Patterns

Polymorphic Batesian mimics exhibit multiple protective morphs that each mimic a different noxious model. Here, we study the genomic transitions leading to the evolution of different mimetic wing patterns in the polymorphic Mocker Swallowtail Papilio dardanus. We generated a draft genome (231 Mb over 30 chromosomes) and re-sequenced individuals of three morphs. Genome-wide single nucleotide polymorphism (SNP) analysis revealed elevated linkage disequilibrium and divergence between morphs in the regulatory region of engrailed, a developmental gene previously implicated in the mimicry switch . The diverged region exhibits a discrete chromosomal inversion (of 40 kb) relative to the ancestral orientation that is associated with the cenea morph, but not with the bottom-recessive hippocoonides morph or with non-mimetic allopatric populations. The functional role of this inversion in the expression of the novel phenotype is currently unknown, but by preventing recombination, it allows the stable inheritance of divergent alleles enabling geographic spread and local coexistence of multiple adaptive morphs.

scholarly journals Synergistic effect of genetic polymorphisms in TLR6 and TLR10 genes on the risk of pulmonary tuberculosis in a Moldavian population

2021 ◽  
pp. 175342592110299
Author(s):  
Alexander Varzari ◽  
Igor V. Deyneko ◽  
Elena Tudor ◽  
Harald Grallert ◽  
Thomas Illig
Keyword(s):  
Pulmonary Tuberculosis ◽  
Interaction Analysis ◽  
P Value ◽  
Fisher Exact Test ◽  
Snp Analysis ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Exact Test ◽  
Pulmonary Tb ◽  
The Republic

Polymorphisms in genes that control immune function and regulation may influence susceptibility to pulmonary tuberculosis (TB). In this study, 14 polymorphisms in 12 key genes involved in the immune response ( VDR, MR1, TLR1, TLR2, TLR10, SLC11A1, IL1B, IL10, IFNG, TNF, IRAK1, and FOXP3) were tested for their association with pulmonary TB in 271 patients with TB and 251 community-matched controls from the Republic of Moldova. In addition, gene–gene interactions involved in TB susceptibility were analyzed for a total of 43 genetic loci. Single nucleotide polymorphism (SNP) analysis revealed a nominal association between TNF rs1800629 and pulmonary TB (Fisher exact test P = 0.01843). In the pairwise interaction analysis, the combination of the genotypes TLR6 rs5743810 GA and TLR10 rs11096957 GT was significantly associated with an increased genetic risk of pulmonary TB (OR = 2.48, 95% CI = 1.62–3.85; Fisher exact test P value = 1.5 × 10−5, significant after Bonferroni correction). In conclusion, the TLR6 rs5743810 and TLR10 rs11096957 two-locus interaction confers a significantly higher risk for pulmonary TB; due to its high frequency in the population, this SNP combination may serve as a novel biomarker for predicting TB susceptibility.

scholarly journals Whole-Genome Single-Nucleotide-Polymorphism Analysis for Discrimination of Clostridium botulinum Group I Strains

2014 ◽  
Vol 80 (7) ◽  
pp. 2125-2132 ◽  
Author(s):  
Narjol Gonzalez-Escalona ◽  
Ruth Timme ◽  
Brian H. Raphael ◽  
Donald Zink ◽  
Shashi K. Sharma
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Clostridium Botulinum ◽  
Toxin Gene ◽  
Polymorphism Analysis ◽  
Snp Analysis ◽  
Whole Genome ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Content Type ◽  
Group I

ABSTRACTClostridium botulinumis a genetically diverse Gram-positive bacterium producing extremely potent neurotoxins (botulinum neurotoxins A through G [BoNT/A-G]). The complete genome sequences of three strains harboring only the BoNT/A1 nucleotide sequence are publicly available. Although these strains contain a toxin cluster (HA+OrfX−) associated with hemagglutinin genes, little is known about the genomes of subtype A1 strains (termed HA−OrfX+) that lack hemagglutinin genes in the toxin gene cluster. We sequenced the genomes of three BoNT/A1-producingC. botulinumstrains: two strains with the HA+OrfX−cluster (69A and 32A) and one strain with the HA−OrfX+cluster (CDC297). Whole-genome phylogenic single-nucleotide-polymorphism (SNP) analysis of these strains along with other publicly availableC. botulinumgroup I strains revealed five distinct lineages. Strains 69A and 32A clustered with theC. botulinumtype A1 Hall group, and strain CDC297 clustered with theC. botulinumtype Ba4 strain 657. This study reports the use of whole-genome SNP sequence analysis for discrimination ofC. botulinumgroup I strains and demonstrates the utility of this analysis in quickly differentiatingC. botulinumstrains harboring identical toxin gene subtypes. This analysis further supports previous work showing that strains CDC297 and 657 likely evolved from a common ancestor and independently acquired separate BoNT/A1 toxin gene clusters at distinct genomic locations.

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