HAdV-36 leads to adipocyte proliferation of adipose tissue through E4orf1 gene, leading to the development of obesity and related diseases. We aimed to investigate the presence and any association of HAdV-36 in non-alcoholic fatty liver disease (NAFLD) patients Methods: The patient group was composed of 116 patients; 30 obese patients with NAFLD (BMI > 30 kg/m2), 30 patients with Diabetes Mellitus (DM)+NAFLD (BMI > 30 kg/m2), 16 patients with NAFLD (BMI < 30 kg/m2), and operated obese group with NAFLD (BMI > 30 kg/m2). The control group comprised 81 non-obese healthy adults. Liver adipose tissue samples were obtained in 30 operated NAFLD patients. HAdV-36-DNA, HAdV-36 neutralizing antibodies, serum lipid, and adipokine levels were analyzed.HAdV-36 neutralizing antibodies (HAdV-36 Ab-positive) were detected in 10/116 and 2/81 participants in the study and control groups, respectively; the difference was statistically significant (p < 0.005). LDL, total cholesterol but not adipokine levels were found to be significantly higher in HadV-36 Ab-positive patients (p < 0.05). While HAdV-36 was identified as a risk factor with OR = 4.11 in univariate analyses, there was no significant difference in binary logistic regression analysis. HAdV-36-DNA was detected in the adipose tissue samples of two patients.We suggest that the presence of HAdV-36 may lead to the development of obesity with the increase in adipose tissue, and diseases such as hyperlipidemia, NAFLD, DM, and metabolic syndrome may develop on the basis of chronic inflammation caused by obesity. Thus, HAdV-36 may be a plausible risk factor for the development of NAFLD.
Abstract Background Herpes simplex virus (HSV) infections are among the most common infectious diseases in humans. The prevalence of herpes simplex viruses type 1 (HSV‐1) and type 2 (HSV‐2) varies widely across the world. HSV‐2 infection is the primary cause of genital herpes. It is highly prevalent in human populations in many parts of the world, and is the most common cause of genital ulcer disease worldwide. In spite of the large prevalence and growing incidence of herpes simplex infection (HSV‐1 and HSV‐2), relatively few data have been published regarding the seroprevalence of herpes simplex infection, while no data exist regarding the Turkish population. Methods We aimed to investigate the prevalence of HSV‐1 and HSV‐2 in selected populations in Turkey. A cross‐sectional study was conducted involving 2082 serum samples of 725 adults, 300 pregnant women, 200 blood donors, 483 sex workers and 110 patients with genital warts and 264 hotel staff in Istanbul, Turkey. All serum samples were assessed for HSV1 and HSV‐2 IgG antibodies using an HSV‐type specific, enzyme‐linked immunosorbent assay (ELISA). Results The prevalence of HSV‐2 and HSV‐1 antibodies was 4.8 and 85.3% in sexually active adults; 5.5 and 96% in blood donors; 5 and 98% in pregnant women, 17.3 and 93.6% in patients with genital warts; 8.3 and 97.3% in hotel staff; and 60% and 99% in sex workers. Conclusion These results confirm a higher prevalence of HSV infection than estimated, especially in high risk groups in Turkey. The high prevalence of HSV infection underlines the need for education among these populations.
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Spontaneous point mutations in genes encoding gyrA/B subunits of DNA gyrase are responsible for fluoroquinolone resistance. We aimed to determine the clarithromycin and levofloxacin resistance phenotypically in H. pylori strains and to investigate the mutations responsible for levofloxacin resistance and the effects of these mutations on dual antibiotic resistance.A total of 65 H. pylori isolates were included. The E-test method was used for the clarithromycin and le-vofloxacin antimicrobial susceptibility test. Real-time PCR was used to detect the point mutations.Twenty-four (36.9%) of 65 H. pylori strains were phenotypically resistant to clarithromycin and 14 (21.5%) to levofloxacin. The phenotypic levofloxacin resistance rate of strains with Asn87Lys and Asp91Asn mutations were significantly higher (gyrA gene) (p < 0.05). The phenotypic levofloxacin resistance rate of strains with Arg484Lys and Asp481Glu mutations were significantly higher (gyrB gene) (p < 0.05). The Asn87Lys mutation increased the risk of phenotypes being resistant to levofloxacin 70.156 times and Asp91Asn mutation increased 125,427 times higher. Seven (10.8%) of 65 H. pylori strains showed dual resistance to both levofloxacin and clarithromycin. The rate of being dual resistant with A2143G mutation (clarithromycin resistance) was found to be significantly higher (p < 0.05).The Asn87Lys and Asp91Asn mutations in the gyrA gene had a phenotypically enhancing effect on levofloxacin resistance, while the presence of Asp481Glu and Arg484Lys mutations in the gyrB gene did not. The existence of dual resistance was developed with the increase in clarithromycin and levofloxacin resistance rates.
Cystic echinococcosis is one of the most important zoonotic diseases in Turkey. The aim of this study was for the molecular analysis of Echinococcus granulosusisolates from different regions of Turkey. For this purpose, 46 hydatid cyst samples collected from humans during the surgery were included. The partial sequences of mitochondrial cytochrome c oxidase subunit 1 (CO1) gene was used for identification and molecular analysis of E. granulosus strains. Molecular analysis showed that all of the human cysts belonged to the G1 genotype (common sheep strain) of E. granulosus. According to the results of our study, the sheep strain (G1) is the predominant genotype of E. granulosus in humans in our country.
Key words: Echinococcus granulosus, human, hydatid cyst, genotype, Turkey.
Background: Porphyromonas gingivalis, a major periodontal pathogen, is gaining increasing attention for its possible association with atherosclerosis. Its fimbriae are classified into six genotypes (Types I-V, Ib) based 0on the diversity of the fim A genes encoding the fimbrial subunits. In this study, fim A genotype's distribution of P. gingivalis was analyzed in atherosclerotic plaque specimens. Methods & Materials: A total of 50 atherosclerotic plaque specimens and 50 non-atherosclerotic, post stenotic aneurysm specimens were collected from patients undergoing cardiovascular surgery. Bacterial DNA was also extracted from each specimen, as real-time PCR was carried out with P. gingivalis-specific primer sets. The positive specimens of P. gingivalis were further analyzed to discriminate the fim A genotype using real-time and nested PCR methods. Results: P. gingivalis was detected only in one atherosclerotic plaque; however, the genotype was nontypable in this specimen. Conclusion: We state that it is not easy to show a significant relationship between P. gingivalis, its fim A genotype, and atherosclerosis. We suggest that new extended studies based especially upon the quantitave determination of P. gingivalis and its genotype distribution on atherosclerotic specimens are needed to show an evident relationship between atherosclerosis and P. gingivalis.
