GBV-B as a pleiotropic virus: distribution of GBV-B in extrahepatic tissues in vivo.

GB virus B (GBV-B) infection of New World monkeys is considered to be a useful surrogate model for hepatitis C virus (HCV) infection. GBV-B replicates in the liver and induces acute resolving hepatitis but little is known whether the other organs could be permissive for the virus. We investigated the viral tropism of GBV-B in tamarins in the acute stage of viral infection and found that the viral genomic RNA could be detected in a variety of tissues.

Identification of novel HCV subgenome replicating persistently in chronic active hepatitis C patients.

In an effort to clarify the life cycle of HCV, the HCV genome in liver biopsies taken from chronic active hepatitis C patients undergoing interferon treatment was investigated. Molecular cloning by long distance reverse-transcription polymerase chain reaction (RT-PCR) revealed that the HCV genome in two patients with high viral loads in the liver had in-frame deletions of approximately 2 kb between E1 and NS2, which encode the E1-NS2 fusion protein and six other HCV proteins: core, NS3, NS4A, NS4B, NS5A, and NS5B. Among the remaining 21 chronic active hepatitis C patients, these types of deletion were found in another two patients and in two hepatocellular carcinoma patients.

Down-regulation of a novel gene, DRLM, in human liver malignancy from 4q22 that encodes a NAP-like protein.

Frequent observations of allelic loss in chromosomal band 4q21-22 in hepatocellular carcinoma (HCC) have suggested the presence of one or more tumor suppressor genes in this region. We screened HCC cell lines by reverse transcription-polymerase chain reaction (RT-PCR) to detect alterations in expression of genes within the region in question by examining expressed sequence tags located there. These experiments identified a full-length cDNA of 2311 bp in length encoding a novel, 182-amino-acid peptide belonging to the class of nucleosome assemble protein lacking nuclear localization signal sequence.