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)

To obtain information about the structure and evolution of the nucleocapsid (N) protein of the coronavirus mouse hepatitis virus (MHV), we determined the entire nucleotide sequences of the N genes of MHV-A59, MHV-3, MHV-S, and MHV-1 from cDNA clones. At the nucleotide level, the N gene sequences of these viral strains, and that of MHV-JHM, were more than 92% conserved overall. Even higher nucleotide sequence identity was found in the 3' untranslated regions (3' UTRs) of the five strains, which may reflect the role of the 3' UTR in negative-strand RNA synthesis. All five N genes were found to encode markedly basic proteins of 454 or 455 residues having at least 94% sequence identity in pairwise comparisons. However, amino acid sequence divergences were found to be clustered in two short segments of N, putative spacer regions that, together, constituted only 11% of the molecule. Thus, the data suggest that the MHV N protein is composed of three highly conserved structural domains connected to each other by regions that have much less constraint on their amino acid sequences. The first two conserved domains contain most of the excess of basic amino acid residues; by contrast, the carboxy-terminal domain is acidic. Finally, we noted that four of the five N genes contain an internal open reading frame that potentially encodes a protein of 207 amino acids having a large proportion of basic and hydrophobic residues.
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PMID:Sequence comparison of the N genes of five strains of the coronavirus mouse hepatitis virus suggests a three domain structure for the nucleocapsid protein. 217 Dec 16

Until 1988 the putative agent of non-A/non-B (NANB) hepatitis had not been found. Research workers of the Chiron Corporation (California, USA) then identified, by "blind expression cloning", polypeptides which specifically bound antibodies present in sera of NANB-patients. A fusion polypeptide (C-100) was expressed in yeast. With the C-100 antigen prototype RIA and ELISA antibody tests were developed. Subsequently more polypeptides (C-200, C33c, C22) of the HCV-genome were added to the test system, resulting in second generation anti-HCV tests with increased sensitivity. For confirmation of HCV ELISA reactive samples, recombinant immunoblot (RIBA-2, Ortho; Innolia, Innogenetics) and dot immunoblot assays (Matrix, Abbott) were developed. Detection of HCV antigens has been hampered by the low virus titres in serum and the absence of free circulating viral antigen(s). However, with cDNA-PCR, applying primers of the highly (> 93% nucleotide homology) conserved 5' untranslated (5'UTR) region of the HCV genome, HCV-RNA in serum as well as in liver tissue can be detected. cDNA-PCR, although not yet commercially available, is useful to confirm HCV-viremia in patients. When chronic hepatitic C patients are treated with anti-viral drugs, the disappearance of HCV-RNA, as detected by PCR, is a measure of therapy response.
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PMID:Testing for HCV markers. 751 61

The role of hepatitis C virus (HCV) infection in fulminant hepatic failure is controversial. The frequency of serum HCV RNA positivity in previously reported patients with fulminant hepatic failure (FHF) of indeterminate cause ranged from 0 to 12% in the United States and Europe and from 43% to 59% in Asia. We assessed serum HCV RNA using polymerase chain reaction (PCR) and oligoprimers from the 5'UTR of the HCV genome in 26 consecutive patients with FHF. Another laboratory independently performed PCR on 21 of the serum samples using different oligoprimers from the 5'UTR and NS3 region of the HCV genome. Serum HCV RNA was detected in two of seven (28%) patients with hepatitis B, 9 of 15 (60%) with an indeterminate cause, and in none with hepatitis A (n = 2) or drug-induced hepatotoxicity (n = 2). HCV RNA PCR results were concordant between both laboratories in 17 of 21 (81%) of samples. In patients with an indeterminate cause, HCV RNA positivity was significantly associated with the transmission risk factor of low socioeconomic status and Hispanic ethnicity. Eighteen patients underwent liver transplantation (LT) and 15 (83%) survived. Among patients with FHF of indeterminate cause, recurrent or acquired HCV infection after transplantation occurred in three of five (60%) and one of four (25%) patients, respectively. Three of four (75%) patients with hepatitis C virus infection post-LT also developed histologic hepatitis. HCV appears to be the causative agent of a substantial number of cases of FHF classified as indeterminate in the Los Angeles area. Differences in patient populations or risk factors may explain the discordant incidences of HCV infection in FHF observed among different programs.
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PMID:Detection of hepatitis C virus with RNA polymerase chain reaction in fulminant hepatic failure. 759 Jun 51

The 3'-end of mouse hepatitis virus (MHV) genomic RNA contains a recognition sequence (55 nucleotides [nt]) required for minus-strand RNA synthesis. To determine whether the 3'-end sequence is also involved in subgenomic mRNA transcription, we have constructed MHV defective interfering (DI) RNAs which contain a chloramphenicol acetyltransferase (CAT) gene placed behind an intergenic sequence and a 3'-end sequence with various degrees of internal deletions. The DI RNAs were transfected into MHV-infected cells, and CAT activities, which represent subgenomic mRNA transcription from the intergenic site, were determined. The results demonstrated that the deletions of sequence upstream of the 350 nt at the 3'-end, which include the 3'-untranslated region (3'-UTR), of MHV genomic RNA did not affect subgenomic mRNA transcription. However, deletions that reduced the 3'-end sequences to 270 nt or less completely abolished the mRNA transcription despite the fact that all of these clones synthesized minus-strand RNAs. These results indicated that mRNA transcription from an intergenic site in the MHV DI RNA requires most of the 3'-UTR as a cis-acting signal, which likely exerts its effects during plus-strand RNA synthesis. A substitution of the corresponding bovine coronavirus sequence for the MHV sequence within nt 270 to 305 from the 3'-end abrogated the CAT gene expression, suggesting a very rigid sequence requirement in this region. The deletion of a putative pseudoknot structure within the 3'-UTR also abolished the CAT gene expression. These findings suggest that the 3'-UTR may interact with the other RNA regulatory elements to regulate mRNA transcription.
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PMID:The 3' untranslated region of coronavirus RNA is required for subgenomic mRNA transcription from a defective interfering RNA. 879 74

Hepatitis C virus (HCV) genotypes were investigated in 57 HCV-infected patients undergoing allogeneic BMT at four European BMT units where death resulting from liver failure (LF) in HCV-infected patients varied from < 1% to > 80%. The aim of the study was to determine whether differing HCV genotypes could account for the different severity of post-transplant liver disease (LD). Sera from patients with pre (n = 22) or post-BMT (n = 35) HCV infection were collected from Italy (Genova, Monza), Sweden (Huddinge) and Germany (Ulm). Patients were grouped as follows: LF: 19/57; acute hepatitis (AH): 10/57 or chronic hepatitis (CH): 22/57; no liver disease (LD): 6/57. HCV genotypes were identified by hybridisation of the 5'UTR amplified products with type-specific oligonucleotides probes according to Simmonds (Hepatology 1994; 19: 1321-1324). Genotype HCV 1 was identified in 34 patients (60%), HCV 2 in 15 (26%), HCV 3 in three (5%), mixed infection in three (5%) and undefined in two (3.5%). In the LF group HCV 1 was identified in 10/19 and other genotypes in 9/19. Median timing of LF was earlier in patients infected with HCV 1 compared to other genotypes (45 and 68 days, respectively), largely due to the cause of LF; death from veno-occlusive disease (VOD) and hepatitis occurred at 30 and 68 days post-BMT, respectively. Genotype 1 was also identified in cases with no LD. These data indicate that there was no evident correlation between HCV genotype and type or severity of post-transplant liver disease.
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PMID:Hepatitis C virus genotypes and liver disease in patients undergoing allogeneic bone marrow transplantation. 902 52

Infection with HGBV-C was surveyed in 286 patients with chronic liver disease. HGBV-C RNA was detected in 19 patients (6.6%), by nested RT-PCR with 5'UTR-derived primers. There were no appreciable differences in clinical and virological features between patients with and without HGBV-C RNA in serum. HGBV-C RNA was detected in three of 83(4%) patients with HBV infection, 15(8%) of 188 patients with HCV infection, and one of 12(8%) patients without evidence of ongoing infection with HBV or HCV, suggesting that the contribution of HGBV-C to non-B non-C hepatitis would not be high. HGBV-C RNA was detected more frequently in the patients with liver cirrhosis or hepatocellular carcinoma than in those with chronic hepatitis. This could reflect a possible role of HGBV-C in aggravating liver disease in co-operation with the other hepatitis viruses.
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PMID:[HGBV-C infection in patients with chronic liver disease]. 908 59

Although a new virus, GB virus C/hepatitis G virus (GBV-C/HGV), has been isolated from patients with hepatitis by two different research groups, its prevalence in the world and pathogenesis are still unknown. In this study, 92 samples from the Jewish population of Uzbekistan were investigated for the prevalence of GBV-C/HGV. GBV-C/HGV RNA was detected by reverse transcription polymerase chain reaction (RT-PCR) using specific primers derived from the 5'-untranslated region (5'-UTR). Sequences were analyzed by a molecular evolutionary method. Of 92 samples, GBV-C/HGV RNA was detected in ten (10.9%), HCV RNA was present in two (2.2%), and HBsAg in eight (8.7%). HTLV-I and HIV infection was not detected. Single GBV-C/HGV infection was detected in eight (80%), and co-infection with HBV or HCV was detected in only two of the GBV-C/HGV infections. Alanine aminotransferase (ALT) levels were elevated in three (3.3%), but none with single GBV-C/HGV infection had an elevated ALT level. Nine people (90%) with GBV-C/HGV infection were distributed under the mean age of the population (P < 0.05). Molecular evolutionary analysis showed all GBV-C/HGV strains in this study were related to the HGV derived from the US. These results indicate that (1) GBV-C/HGV infection is highly prevalent among the Jewish population in Uzbekistan; (2) single GBV-C/HGV infections without persistent hepatitis are common; and (3) GBV-C/HGV infection is present among the younger generation.
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PMID:High prevalence of GB virus C/hepatitis G virus infection among the Jewish population in Uzbekistan. 914 Jan 96

The presence of hepatitis GB virus C (GBV-C), also known as hepatitis G virus (HGV), and hepatitis C virus (HCV) were investigated in sera from 45 hemophiliacs from nine locations in Nicaragua using a nested polymerase chain reaction (PCR). Primers used to detect GBV-C and HCV derived from the helicase region and 5'UTR, respectively. Seventeen (38%) patients were positive for GBV-C RNA in serum by PCR. Twelve (27%) patients were positive for HCV RNA by PCR. Six (13%) of these were coinfected with GBV-C. Anti-HCV was detected in all the 12 HCV RNA positive hemophiliacs and in another 14 (31%) individuals, in whom GBV-C RNA was found in 2. Ten patients (22%) lacked markers for both GBV-C and HCV. The mean age of the patients positive for GBV-C but negative for HCV by PCR was significantly lower than for those negative for GBV-C but positive for HCV by PCR (P < 0.05; Student's t-test), indicating that the risk for this group of hemophiliacs to acquire GBV-C infection is higher as compared to the risk of acquiring HCV infection. Eleven GBV-C strains were sequenced in the 5'UTR. Sequence comparison to previously published GBV-C strains revealed that all 11 strains were more similar to Asian strains than to strains of European and African origin. Sequences in the NS5-B region were available for 8 HCV strains, all of which were found to belong to genotype 1a. The similarity of the Nicaraguan GBV-C strains to strains from Asia indicates that the GBV-C strains in the region presumably have an Amerindian origin. It is also considered that the HTLV II strains in the New World aboriginal populations are ancient and brought there by the ancestral Amerindian populations from Asia. Further, the genotype F of hepatitis B virus, known to represent the strains in populations with Amerindian background, predominates in Central American populations with Hispanic background. It remains to be clarified why Amerindian strains of GBV-C as well as of HBV predominate also in populations with mixed ethnic background in Central America.
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PMID:High prevalence of GB virus C strains genetically related to strains with Asian origin in Nicaraguan hemophiliacs. 917 60

The genetic diversity of hepatitis G virus (HGV) was investigated. By using a RT-PCR procedure, 14% of either HBV (hepatitis B virus)- or HCV (hepatitis C virus)-positive Korean hepatitis patients were proved to be HGV positives. Nucleotide sequences in the E1 region of the eight isolates from Korean patients and the six previously reported isolates were compared. Nucleotide substitutions spread uniformly throughout the E1 region. Sequence homology among the Korean isolates was 84-99% and 88-99% at the nucleotide and amino acid sequences, respectively, whereas those from different geographic areas was slightly lower at both levels. At least two genotypes might exist among the Korean HGV isolates. Compared to the corresponding region of HCV, the E1 sequence from HGV is moderately conserved. In addition, as frameshift mutations were observed in most of the Korean isolates compared to the prototype HGV sequence, the Korean isolates might not use the translational initiation site of the prototype HGV for polyprotein translation. Because a putative signal sequence of E1 for entry into endoplasmic reticulum starts from the N-terminus of the polyprotein, and capsid-like peptides composed of basic amino acids could not be detected from the upstream region of E1, the core protein of HGV is absent, or at least not present, at the region next to 5'-UTR. Therefore, HGV could be clearly distinguished from other genera of Flaviviridae.
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PMID:Analysis of the envelope region of hepatitis G virus isolated from Korean patients. 957 42

The 3' untranslated regions (3' UTRs) of coronaviruses contain the signals necessary for negative strand RNA synthesis and may also harbor elements essential for positive strand replication and subgenomic RNA transcription. The 3' UTRs of mouse hepatitis virus (MHV) and bovine coronavirus (BCV) are more than 30% divergent. In an effort to learn what parts of these regions might be functionally interchangeable, we attempted to replace the 3' UTR of MHV with its BCV counterpart by targeted RNA recombination. Initially, we tried to substitute the 3' 267 nucleotides (nt) of the 301 nt MHV 3' UTR with the corresponding region of the BCV 3' UTR. This exchange did not yield viable recombinant viruses, and the donor DI RNA was shown to be unable to replicate with MHV as a helper virus. Subsequent analysis revealed that the entire BCV 3' UTR could be inserted into the MHV genome in place of the entire MHV 3' UTR. It resulted that the failure of the initial attempted substitution was due to the inadvertent disruption of an essential conserved bulged stem-loop secondary structure in the MHV and BCV 3' URTs immediately downstream of the N gene stop codon.
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PMID:An essential secondary structure in the 3' untranslated region of the mouse hepatitis virus genome. 978 96


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