128 research outputs found

    Impact of River Morphological Changes on Floodplain Vegetation

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    Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

    An Experimental Study on Bed Degradation Due to Falling Works Improvement

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    Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

    Analysis of 5′ Nontranslated Region of Hepatitis A Viral RNA Genotype I from South Korea: Comparison with Disease Severities

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    The aim of the study was to analyze genotype I hepatitis A virus (HAV) 5′ nontranslated region (NTR) sequences from a recent outbreak in South Korea and compare them with reported sequences from Japan. We collected a total of 54 acute hepatitis A patients' sera from HAV genotype I [27 severe disease (prothrombin time INR≥1.50) and 27 mild hepatitis (prothrombin time INR <1.00)], performed nested RT-PCR of 5′ NTR of HAV directly sequenced from PCR products (∼300 bp), and compared them with each other. We could detect HAV 5′NTR sequences in 19 of the 54 (35.1%) cases [12 of 27 severe cases (44.4%) and 7 of 27 self-limited cases (25.9%)], all of which were subgenotype IA. Sequence analysis revealed that sequences of severe disease had 93.6%–99.0% homology and of self-limited disease 94.3%–98.6% homology, compared to subgenotype IA HAV GBM wild-type IA sequence. In this study, confirmation of the 5′NTR sequence differences between severe disease and mild disease was not carried out. Comparison with Japanese HAV A10 revealed 222C to G or T substitution in 8/12 cases of severe disease and 222C to G or T and 392G to A substitutions in 5/7 and 4/7 cases of mild disease, respectively, although the nucleotide sequences in this study showed high homology (93.6%–100%). In conclusion, HAV 5′NTR subgenotype IA from Korea had relatively high homology to Japanese sequences previously reported from Japan, and this region would be considered one of the antiviral targets. Further studies will be needed

    Analysis of 5′ Nontranslated Region of Hepatitis A Viral RNA Genotype I from South Korea: Comparison with Disease Severities

    Get PDF
    The aim of the study was to analyze genotype I hepatitis A virus (HAV) 5′ nontranslated region (NTR) sequences from a recent outbreak in South Korea and compare them with reported sequences from Japan. We collected a total of 54 acute hepatitis A patients' sera from HAV genotype I [27 severe disease (prothrombin time INR≥1.50) and 27 mild hepatitis (prothrombin time INR <1.00)], performed nested RT-PCR of 5′ NTR of HAV directly sequenced from PCR products (∼300 bp), and compared them with each other. We could detect HAV 5′NTR sequences in 19 of the 54 (35.1%) cases [12 of 27 severe cases (44.4%) and 7 of 27 self-limited cases (25.9%)], all of which were subgenotype IA. Sequence analysis revealed that sequences of severe disease had 93.6%–99.0% homology and of self-limited disease 94.3%–98.6% homology, compared to subgenotype IA HAV GBM wild-type IA sequence. In this study, confirmation of the 5′NTR sequence differences between severe disease and mild disease was not carried out. Comparison with Japanese HAV A10 revealed 222C to G or T substitution in 8/12 cases of severe disease and 222C to G or T and 392G to A substitutions in 5/7 and 4/7 cases of mild disease, respectively, although the nucleotide sequences in this study showed high homology (93.6%–100%). In conclusion, HAV 5′NTR subgenotype IA from Korea had relatively high homology to Japanese sequences previously reported from Japan, and this region would be considered one of the antiviral targets. Further studies will be needed

    Inhibitory effects on HAV IRES-mediated translation and replication by a combination of amantadine and interferon-alpha

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    Hepatitis A virus (HAV) causes acute hepatitis and sometimes leads to fulminant hepatitis. Amantadine is a tricyclic symmetric amine that inhibits the replication of many DNA and RNA viruses. Amantadine was reported to suppress HAV replication, and the efficacy of amantadine was exhibited in its inhibition of the internal ribosomal entry site (IRES) activities of HAV. Interferon (IFN) also has an antiviral effect through the induction of IFN stimulated genes (ISG) and the degradation of viral RNA. To explore the mechanism of the suppression of HAV replication, we examined the effects of the combination of amantadine and IFN-alpha on HAV IRES-mediated translation, HAV replicon replication in human hepatoma cell lines, and HAV KRM003 genotype IIIB strain replication in African green monkey kidney cell GL37. IFN-alpha seems to have no additive effect on HAV IRES-mediated translation inhibition by amantadine. However, suppressions of HAV replicon and HAV replication were stronger with the combination than with amantadine alone. In conclusion, amantadine, in combination of IFN-alpha, might have a beneficial effect in some patients with acute hepatitis A
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