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  1. Ana Sayfa
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Yazar "Sertöz R." seçeneğine göre listele

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  • Küçük Resim Yok
    Öğe
    Analysis of hepatitis B virus (HBV) preS1, preS2 and S gene regions from patient groups infected with HBV genotype D [Hepatit B Virüsü (HBV) Genotip D ile Enfekte Hasta Gruplarinda HBV preS1, preS2 ve S Gen Bölgelerinin Analizi]
    (Ankara Microbiology Society, 2018) Karataş E.; Erensoy S.; Akarca U.S.; Sertöz R.
    Mutations in preS and S gene regions of hepatitis B virus genome may cause immune escape and diagnostic escape HBV mutants. The aim of this study was to determine preS1, preS2 and S gene regions of HBV from HBV infected patient groups by sequence analysis and contribute to the relevant literature. Nucleic acid sequence analysis of preS and S genes of HBV PCR products from 56 archived plasma samples sent to Ege University Faculty of Medicine Medical Microbiology Department Molecular Virology laboratory, for HBV tests were determined by chain termination reaction. Amino acid (aa) sequences were compared with the reference sequences obtained from GenBank. Plasma samples belonged to four groups of patients: A-Chronic HBV infected patients with typical HBV serological profiles (22 samples), B-HBV infected patients with atypical HBV serological profiles (26 samples), C-HBV re-infected patients after liver transplantation (5 samples), D-Seroconversion phase following acute HBV infection (3 samples). One of two vaccine escape mutant samples was also diagnostic escape mutant; the other diagnostic escape mutant was isolated from anti-HBc positive sample. All of the sequences were determined as genotype D. HBsAg subtypes were determined as; two aywl, six ayw3, two mix, 46 ayw2. Among the 304 codons analysed between preS 33rd and S 162nd amino acids; aa variants were determinedin 105 codons (34.5%). Sequences can be found in GenBank with accession numbers FJ001941-FJ001996. At least one aa variation was detected in 48 of 56 samples (85.7%). The amino acid variants were as follows; PreS1: A33T, A39T, P41K, D44del, D50N, T51P, D54N, L65P/M, F67L, W77T, A81S, Q82E, I84T, L85I/M, Q86H/T, L88S, A90T/V, N91K/del, A95P, S96A, T97I/A, N98K, Q100K, S101T, S109T, P110S, N114D/E, PreS2: M1V, Q2R, S5H, F8S, H9Q, Q13L, D14N, R16K, R18K, G19S/D, F22L/S, S28T, G30E, N33T, V39A, P41H/L, I42T/L, I45T, F46Y, S47L, R48K, I49T, D51V/G, P52L, A53V, L54R/G, N55K; S gene: E2D, I4F, F8L, G10A, VI4A, F20S, L22del, R24K, P29L, Q30K, N40S, F41del, G44E, T45L, T46P, V47A, L49R, Q54R, P56L, S64F, P70A, M75I, C76Y, R79H, 181 T, F83C, L88P, L94S, Y100F, Q101H/R, M103L, LI 04F, LI091/M, I110L, G112S/R, S113N/P, S114A/del, Tl 151, T116N, T118A/K, PI 20A/T, T123A, in "a" determinant; T126I, Q129H/R, T131N, M133T, Y134N, S136Y, S143L/M/T, D144E, G145A/R. Deletions were also found in all three preS/S gene regions. The highest number of aa variations were detectedin the isolated anti-HBc positive sample (in 24 codons), followed by liver transplant group (8-13 codons). Point mutation was detected in the preS2/S promoter CCAAT box. Major hydrophilic region (MHR) variants were determined in 41.1% of 56 samples. The highest number of MHR variants belonged to atypical HBV serological profile group (group B; 61.5%) and liver transplantation group with HBV re-infection (all C group). Among the diagnostic escape and immune escape mutant (anti-HBs positive) samples, reported MHR and "a" determinant mutations were detected. In conclusion, the study population carries HBV preS/S variants; MHR and "a" determinant variant rates are high among diagnostic or immune escape mutants. It is important to evaluate the mutant detection performance of HBsAg tests. © 2018 Ankara Microbiology Society. All rights reserved.
  • Küçük Resim Yok
    Öğe
    A case of chronic hepatitis B with primary adefovir resistance [Adefovire primer dirençli bir kronik B hepatiti olgusu]
    (2007) Yamazhan T.; Sertöz R.; Pullukçu H.; Taşbakan M.; Ulusoy S.; Erensoy S.
    Implementation of antiviral therapy leads to the emergence of mutant strains during the treatment in chronic hepatitis B. Hepatitis B virus (HBV) with primary antiviral resistance may be rarely encountered. In this report, a chronic hepatitis B case who had never received adefovir dipivoxil but had primary adefovir resistance, was presented. HBeAg positive 25-year-old male patient was treated with interferon (IFN)-alpha (thrice a week 10 MU) and lamivudine (100 mg/daily) combination for one year. At the end of this treatment although HBV-DNA was under the detectable limit and ALT levels returned to normal, anti-HBe antibodies did not develop. During the course of lamivudin treatment on the third year virus was found to be resistant to lamivudin [FLM+YMDD+YIDD+YVDD (Inno-LiPA HBV DR, Innogenetics Ghent, Belgium)] and adefovir was added to the lamivudin therapy. At the end of eight months of combination therapy, ALT levels did not return to normal and HBV-DNA was still in detectable levels. On the 11th month resistance to adefovir was analysed and rtA181T mutation was found by DNA sequence analysis (Big Dye Terminator Cycle Sequencing kit, Applied Biosystems, USA). Since there had been no response to adefovir from the initiation of the therapy, primary adefovir resistance was suspected. Primary adefovir resistance was confirmed by the detection of the same mutation in pre-adefovir treatment serum sample of the patient. Lamivudin was re-added to the therapy, however, HBV-DNA still remained positive on the third month of this combination therapy. The patient got out of routine follow-up after this period.
  • Küçük Resim Yok
    Öğe
    Investigation of anti-htlv-i/ii seroprevalence in healthy blood donors in Izmir region, Turkey [Izmir bölgesinde saglikli kan verícílerínde antí-HTLV-I/II seroprevalansinin araçtirilmasi]
    (2010) Sertöz R.; Turhan A.; Bozkurt H.; Çamlioglu P.; Degrmenci A.; Aydinok Y.; Erensoy S.
    Almost 10-20 million people in the world are thought to be infected by human deltaretroviruses, namely human T-cell lymphotropic virus (HTLV) type I and II, recently. HTLV-I is endemic in southwestern Japan, the Caribbean and sub-Saharan Africa, whereas HTLV-II is more prevalent in intravenous drug addicts, and in American indián populations, endemically. HTLV-I is mainly responsible for adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), however, HTLVII is not clearly associated with a known clinical disease. Both viruses may be transmitted by sexual contact, parenteral route, whole blood transfusion and breast-feeding. In most of the countries [USA, Canada, South America, Caribbean, Japan, Taiwan and some Europe countries (France, UK, Ireland, Sweden, Denmark, The Netherlands, Portugal, Romania, Greece)] routine screening of anti-HTLV-I/II in blood donors is mandatory, however, there is no such practice in Turkey since seroepidemiologic data on HTLVI/II infections is insufficient. In this study, the seroprevalence of HTLV-I/II in healthy blood donors admitted to the blood bank of Ege University Medical Faculty Hospital, Izmir (located at Aegean region), was investigated to support data on the decision making process on routine screening of anti-HTLV-I/II in blood centers. Serum samples from 10.000 healthy blood donors (mean age: 32.6 years; 87.8% were male), who succeeded the donor history questionnaire, were included to the study, and HTLV-I/II antibodies were screened by a commercial enzyme immunoassay (ELISA) (Murex HTLVI-II, Murex Diagnostics, UK) method. Serum samples which were yielded reactive and borderline results were retested by ELISA, and repeated reactive/borderline results were then confirmed by HTLV-I/II confirmation test (INNO-LIA HTLV-I/II, lnnogenetics, Belgium). Seven samples yielded reactive/borderline reactive results by both ELISA lots, however, all of them were found negative by confirmatory test. According to our data HTLV-I/II infections are not endemic in Izmir region, and anti-HTLV-I/II screening of blood donors is not required in our blood center currently. Nevertheless, screening HIV which is very rare in prevalence among the donor population, is mandatory for blood donors in our country. Thus, even its prevalence is very low, much more comprehensive and multi-centered studies are necessary for making the decision of integrating HTLV-I/II in routine blood bank screening tests in Turkey.
  • Küçük Resim Yok
    Öğe
    Role of line immunoassay in the diagnosis of early HIV Infection: A diagnostic case [Erken dönem hiv enfeksiyonunda line immunoassay testinin yeri: Tanisal bir olgu]
    (2013) Soylar M.; Altuclu I.; Sertöz R.; Gökengin D.
    Combined p24 antigen-HIV antibody fourth-generation assays that identify most of the earty HIV infections have been used extensively worldwide for several years. This poses challenges for the traditional algorithm of line immunoassay (LIA) confirmation. UA tests are useful methods with their high specificity and their ability to differentiate HIV-1 from HIV-2, but they are reactive days after the fourth generation enzyme immunoassays. With acute HIV infection, high levels of infectious virus are detectable in serum and genital secretions. The rate of transmission during acute HIV infection is higher than the established HIV infection, for this reason, new HIV testing strategies need to focus on sensitivity, especially for this highly contagious phase immediately after infection. Serum sample of a patient sent to Ege University Hospital Clinical Virology Laboratory was repeatedly reactive with low signal/cutoff ratios with two different commercial fourth generation enzyme immunoassays (Architect HIV Ag/Ab Combo Reagent Kit, Abbott, Germany and Vidas HIV Duo Quick, Biomerieux, France). The sample was non-reactive with the LIA (INNO-UA HIV I/ll Score, lnnogenetics, Belgium) and HIV RNA (RealTime HIV-I Amplification Reagent Kit, Abbott, USA) result was positive (4.1 × 105 copies/ml). With the presentation of this case, the role of UA in the diagnosis of earty HIV infection and its place in test algorithms were questioned.

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