Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Further modifications of the structural features of Schiff bases of hydroxyaminoguanidines (SB-HAG) led to nine substituted salicylaldehyde Schiff bases of HAG (SSB-HAG) derivatives and three other SB-HAG derivatives. These new compounds were tested for the first time against infection by a coronavirus, mouse hepatitis virus (MHV). The most active compound, 2 [1-[(3'-allyl-2'-hydroxybenzylidene)amino]- 3-hydroxyguanidine], against the growth of MHV is about 376 times more active than hydroxyguanidine and about 564 times more active than HAG itself when the TCID50 values are compared. Plaque assays of MHV released from cells treated with these compounds suggest that SSB-HAG tosylate may inhibit the transcription of viral RNAs in virus-infected cells. Quantitative structure-activity relationship (QSAR) analyses of two subsets show that the inhibitory activities correlate well with the electronic and the lipophilic parameters. The structural requirements for the antiviral activity of substituted SSB-HAG tosylate against coronaviral infection are stringent according to the inhibitory activities and QSAR analysis of these new compounds.
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PMID:Design, synthesis, testing, and quantitative structure-activity relationship analysis of substituted salicylaldehyde Schiff bases of 1-amino-3-hydroxyguanidine tosylate as new antiviral agents against coronavirus. 215 21

A novel method was developed to assemble a full-length infectious cDNA of the group II coronavirus mouse hepatitis virus strain A59 (MHV-A59). Seven contiguous cDNA clones that spanned the 31.5-kb MHV genome were isolated. The ends of the cDNAs were engineered with unique junctions and assembled with only the adjacent cDNA subclones, resulting in an intact MHV-A59 cDNA construct of approximately 31.5 kb in length. The interconnecting restriction site junctions that are located at the ends of each cDNA are systematically removed during the assembly of the complete full-length cDNA product, allowing reassembly without the introduction of nucleotide changes. RNA transcripts derived from the full-length MHV-A59 construct were infectious, although transfection frequencies were enhanced 10- to 15-fold in the presence of transcripts encoding the nucleocapsid protein N. Plaque-purified virus derived from the infectious construct replicated efficiently and displayed similar growth kinetics, plaque morphology, and cytopathology in murine cells as did wild-type MHV-A59. Molecularly cloned viruses recognized the MHV receptor (MHVR) for docking and entry, and pretreatment of cells with monoclonal antibodies against MHVR blocked virus entry and replication. Cells infected with molecularly cloned MHV-A59 virus expressed replicase (gene 1) proteins identical to those of laboratory MHV-A59. Importantly, the molecularly cloned viruses contained three marker mutations that had been derived from the engineered component clones. Full-length infectious constructs of MHV-A59 will permit genetic modifications of the entire coronavirus genome, particularly in the replicase gene. The method has the potential to be used to construct viral, microbial, or eukaryotic genomes approaching several million base pairs in length and used to insert restriction sites at any given nucleotide in a microbial genome.
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PMID:Systematic assembly of a full-length infectious cDNA of mouse hepatitis virus strain A59. 1236 49

Pyrrolo[2,3-d]pyrimidine and tetrazolopyrimidine derivatives 2a, b-5a, b were prepared. Also, acyclic and cyclic C-nucleosides 7a, b-12a, b were prepared by treating compound 6 with some aldoses. All prepared products were tested for antiviral activity against hepatitis-A virus (HAV, MBB-cell culture adapted strain) and herpes simplex virus type-1 (HSV-1). Plaque reduction infectivity assay was used to determine virus count reduction as a result of treatment with tested compounds. Compound 2a showed the highest effect on HAV, while compound 11b showed the highest effect on the HSV-1 virus.
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PMID:Synthesis and biological evaluation of some pyrrolo[2,3-d]pyrimidines. 1714 93

Sugar N-arylaminoacetylhydrazones 2-5 were prepared by the reaction of N-arylaminoacetylhydrazides 1 with equivalent amounts of the corresponding monosaccharides. Per-O-acetyl derivatives 6-9 of sugar hydrazones 2-5 were prepared by using acetic anhydride in pyridine at room temperature, while on boiling with acetic anhydride, cyclization had taken place to give the oxadiazolines 10-12. The prepared compounds were tested for antiviral activity against Herpes Simplex virus type-1 (HSV-1) and hepatitis-A virus (HAV, MBB-cell culture adapted strain). Plaque reduction infectivity assay was used to determine virus count reduction as a result of treatment with tested compounds.
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PMID:Synthesis and antiviral evaluation of some sugar arylglycinoylhydrazones and their oxadiazoline derivatives. 1714 95

6-Phenyl-[1,2,4]triazolo[4,3-b]pyridazine-3(2H)-thione 2 was used as precursor for the preparation of some novel 3-S-substituted-6-phenyl-[1,2,4]triazolo[4,3-b]pyridazine derivatives 3-11. Furthermore, the preparation of 1-[2-(6-phenyl-[1,2,4]triazolo[4,3-b]pyridazin-3-ylsulfanyl)-acetyl]-1H-pyrazole derivative 13 and 5-(6-phenyl-[1,2,4]triazolo[4,3-b]pyridazin-3-ylsulfanylmethyl)-[1,3,4]oxadiazole derivatives 15 and 17, are described. Some of the prepared products revealed a promising antiviral activity against hepatitis-A virus (HAV, MBB-cell culture adapted strain). Plaque reduction infectivity assay was used to determine virus count reduction as a result of treatment with the test compounds. Compound 15 showed the highest effect on HAV compared to the other tested compounds.
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PMID:Anti-HAV activity of some newly synthesized triazolo[4,3-b]pyridazines. 1821 48

Plaque assays for virulent and attenuated duck hepatitis virus (DHV) type I in duck embryo liver (DEL) and duck embryo kidney (DEK) cells are described. The results of assays for DHV type I strains by in vitro, in ovo and in vivo methods are compared. DHV type II and III did not produce plaques in DEL or DEK cells. A serological relationship between DHV type I and DHV type II and III could not be demonstrated by the plaque reduction neutralisation assay.
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PMID:An assay for duck hepatitis virus type I in duck embryo liver cells and a comparison with other assays. 1876 6