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    SARS-CoV-2 Mutations and their Viral Variants
    (2022) Cosar, Begum; Karagulleoglu, Zeynep Yagmur; Unal, Sinan; Ince, Ahmet Turan; Uncuoglu, Dilruba Beyza; Tuncer, Gizem; Kilinc, Bugrahan Regaip; Ozkan, Yunus Emre; Ozkoc, Hikmet Ceyda; Demir, Ibrahim Naki; Eker, Ali; Karagoz, Feyzanur; Simsek, Said Yasin; Yasar, Bunyamin; Pala, Mehmetcan; Demir, Aysegul; Atak, Irem Naz; Mendi, Aysegul Hanife; Bengi, Vehdi Umut; Sevel, Guldane Cengiz; Altuntas, Evrim Gunes; Kilic, Pelin; Demir-Dora, Devrim; https://orcid.org/0000-0003-0359-6308; 34580015
    Mutations in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) occur spontaneously during replication. Thousands of mutations have accumulated and continue to since the emergence of the virus. As novel mutations continue appearing at the scene, naturally, new variants are increasingly observed.Since the first occurrence of the SARS-CoV-2 infection, a wide variety of drug compounds affecting the binding sites of the virus have begun to be studied. As the drug and vaccine trials are continuing, it is of utmost importance to take into consideration the SARS-CoV-2 mutations and their respective frequencies since these data could lead the way to multi-drug combinations. The lack of effective therapeutic and preventive strategies against human coronaviruses (hCoVs) necessitates research that is of interest to the clinical applications.The reason why the mutations in glycoprotein S lead to vaccine escape is related to the location of the mutation and the affinity of the protein. At the same time, it can be said that variations should occur in areas such as the receptor-binding domain (RBD), and vaccines and antiviral drugs should be formulated by targeting more than one viral protein.
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    Alpha-Thalassemia Mutations in Adana Province, Southern Turkey: Genotype-Phenotype Correlation
    (2015) Bozdogan, Sevcan Tug; Yuregir, Ozge Ozalp; Buyukkurt, Nurhilal; Aslan, Huseyin; Ozdemir, Zeynep Canan; Gambin, Tomasız; 25825562
    To look over the distribution of the mutations in a large series from Adana province, Southern Turkey, and determine the genotype-phenotype correlation of the frequent mutations. Among the 2500 individuals with mild or moderate anemia, microcytosis, and normal iron levels that were referred to our Genetic Diagnosis Center, a population consisting of 539 individuals were included in the study and tested for alpha-thalassemia mutations by using reverse dot blot hybridization technique. Twelve different mutations were detected in 539 patients. Among the 12 different mutations found, the most frequent mutations were the -alpha(3.7) (63.3 %), --(MED) (11.7 %), --(20.5) (10.7 %), alpha 2(IVS1(-5nt)) (3.9 %), and alpha 2(polyA-2) (3.5 %). The most frequent genotypes were -alpha(3.7)/alpha alpha (35.8 %), -alpha(3.7)/-alpha(3.7)(18.9 %), -(20.5)/alpha alpha (11.5 %), and --(MED)/alpha alpha (10.4 %), respectively. There were statistically significant differences in hematological findings between -alpha(3.7)/-alpha(3.7) and --(MED)/alpha alpha, even though both have two mutated genes in the genotype. Our results show that alpha-thalassemia mutations are highly heterogeneous as well as deletional and -alpha(3.7) single gene deletion is particularly prevalent at Adana province in agreement to other studies from Turkey.