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Specific interaction of eukaryotic translation initiation factor 3 with the 5' nontranslated regions of hepatitis C virus and classical swine fever virus RNAs.

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Translation of hepatitis C virus (HCV) and classical swine fever virus (CSFV) RNAs is initiated by cap-independent attachment (internal entry) of ribosomes to the approximately 350-nucleotide internal ribosomal entry segment (IRES) at the 5' end of both RNAs. Eukaryotic initiation factor 3 (eIF3)

Yellow fever 5' noncoding region as a potential element to improve hepatitis C virus production through modification of translational control.

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The lengthy 5' noncoding region (5' NCR) of hepatitis C virus (HCV) RNA forms a highly ordered secondary structure, very conserved among different strains. It includes an internal ribosome entry site (IRES) element, responsible for the cap-independent translation initiation of HCV RNA. Similarly to

Analysis of hepatitis C virus/classical swine fever virus chimeric 5'NTRs: sequences within the hepatitis C virus IRES are required for viral RNA replication.

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Hepatitis C virus (HCV) is classified in the genus Hepacivirus of the family Flaviviridae, whose members have a single-stranded RNA genome of positive polarity, which encodes a single polyprotein. Within this family, HCV is closely related to viruses of the genus Pestivirus, which includes classical

Acute Q fever presenting as antiphospholipid syndrome, pneumonia, and acalculous cholecystitis and masquerading as Mycoplasma pneumoniae and hepatitis C viral infections.

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We report a case of Q fever-related antiphospholipid syndrome in a patient presenting with acalculous cholecystitis and pneumonia. Serial laboratory tests indicated that the previous serological tests suggesting hepatitis C virus and Mycoplasma pneumoniae infections were false-positives. The

[Prevalence of hepatitis C antibodies in plasma donors for the treatment of Argentine hemorrhagic fever].

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For Argentine Hemorrhagic Fever, a disease caused by Junin virus (JV), there is an effective treatment, consisting of the transfusion of immune plasma (IP). This plasma is obtained from individuals who have had the disease. Since Hepatitis C virus (HCV) is transmitted parenterally, this study was

Long-term familial Mediterranean fever remission on successful hepatitis C virus treatment in a patient not responding to colchicine: a case report.

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BACKGROUND Familial Mediterranean fever is an autosomal recessive disorder characterized by periodic febrile attacks of aseptic serositis and/or arthritis. The main treatment is colchicine which prevents attacks in the majority of patients except for a group of colchicine-resistant cases. Chronic

Synergistic in vitro interactions between alpha interferon and ribavirin against bovine viral diarrhea virus and yellow fever virus as surrogate models of hepatitis C virus replication.

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Monotherapy of hepatitis C virus infection with either alpha interferon or ribavirin alone is rather ineffective, while the use of the two antivirals together is much more efficacious. In vitro drug-drug combination analysis utilizing related members of the family Flaviviridae, bovine viral diarrhea

Human antibodies to dengue and yellow fever do not react in diagnostic assays for hepatitis C virus.

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Hepatitis C virus (HCV) is a recently described causative agent of the great majority of post-transfusion non A-non B hepatitis and is classified within the Flaviviridae family. Due to a high prevalence of anti-HCV and other flaviviruses circulating in Brazil, such as dengue and yellow fever, we

Phospholipidomic identification of potential serum biomarkers in dengue fever, hepatitis B and hepatitis C using liquid chromatography-electrospray ionization-tandem mass spectrometry.

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The serum phospholipid (PL) profiles of healthy volunteers (HE) and patients with recently diagnosed dengue fever (DF), hepatitis B (HBV), and hepatitis C (HCV) were investigated using liquid chromatography-ion trap-mass spectrometry (LC-IT-MS) and liquid chromatography-triple quad-mass spectrometry

A prokaryotic-like mode of cytoplasmic eukaryotic ribosome binding to the initiation codon during internal translation initiation of hepatitis C and classical swine fever virus RNAs.

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Initiation of translation of hepatitis C virus and classical swine fever virus mRNAs results from internal ribosomal entry. We reconstituted internal ribosomal entry in vitro from purified translation components and monitored assembly of 48S ribosomal preinitiation complexes by toe-printing.

Novel thioglycosyl analogs of glycosyltransferase substrates as antiviral compounds against classical swine fever virus and hepatitis C virus.

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Hepatitis C virus (HCV) and classical swine fever virus (CSFV) are important pathogens for which new therapeutic approaches are in high demand. Herein, we report the synthesis of newly designed thioglycosyl analogs of glycosyltransferase substrates which were evaluated using cell-based assays for

Yellow fever virus replicons as an expression system for hepatitis C virus structural proteins.

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Chimeric yellow fever virus (YF) RNAs were constructed in which the YF structural genes were replaced by the hepatitis C virus (HCV) structural genes or fusions between the YF and HCV structural genes. Interestingly, RNA replication required nucleotide complementarity between the 3'-located

[Hepatitis C virus infection mimicking hemorrhagic fever: a case report]

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Acute C hepatitis, compared with hepatitis A or B, may sometimes be associated with extrahepatic manifestations of a haematologic nature. The first case of hepatitis associated with aplastic anemia was reported by Lorenz in 1955. We observed a patient who developed acute hepatitis, associated with

Acute non-A non-B hepatitis after typhoid fever.

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Female sex and IL28B, a synergism for spontaneous viral clearance in hepatitis C virus (HCV) seroconverters from a community-based cohort.

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OBJECTIVE Since acute hepatitis C virus (HCV) infection is often asymptomatic, it is difficult to examine the rate and determinants of spontaneous clearance. Consequently, these studies are subject to bias, which can potentially lead to biased rates of viral clearance and risk estimates. We

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