Linsheng Guo
Baylor University Medical Center
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Publication
Featured researches published by Linsheng Guo.
Proceedings of the National Academy of Sciences of the United States of America | 2003
Lizhe Xu; Zhiwei Shen; Linsheng Guo; Brent Fodera; Adrian Keogh; Ruth Joplin; Barbara O'Donnell; James Aitken; William F. Carman; James Neuberger; Andrew L. Mason
Patients with primary biliary cirrhosis develop progressive ductopenia associated with the production of antimitochondrial antibodies that react with a protein aberrantly expressed on biliary epithelial cells and peri-hepatic lymph nodes. Although no specific microbe has been identified, it is thought that an infectious agent triggers this autoimmune liver disease in genetically predisposed individuals. Previous serologic studies have provided evidence to suggest a viral association with primary biliary cirrhosis. Here we describe the identification of viral particles in biliary epithelium by electron microscopy and the cloning of exogenous retroviral nucleotide sequences from patients with primary biliary cirrhosis. The putative agent is referred to as the human betaretrovirus because it shares close homology with the murine mammary tumor virus and a human retrovirus cloned from breast cancer tissue. In vivo, we have found that the majority of patients with primary biliary cirrhosis have both RT-PCR and immunohistochemistry evidence of human betaretrovirus infection in lymph nodes. Moreover, the viral proteins colocalize to cells demonstrating aberrant autoantigen expression. In vitro, we have found that lymph node homogenates from patients with primary biliary cirrhosis can induce autoantigen expression in normal biliary epithelial cells in coculture. Normal biliary epithelial cells also develop the phenotypic manifestation of primary biliary cirrhosis when cocultivated in serial passage with supernatants containing the human betaretrovirus or the murine mammary tumor virus, providing a model to test Kochs postulates in vitro.
Gene | 2000
Raleigh D. Kladney; Gary A. Bulla; Linsheng Guo; Andrew L. Mason; Ann E. Tollefson; Daniela J. Simon; Zaher Koutoubi; Claus J. Fimmel
Abstract We report the isolation and characterization of GP73, a novel 73kDa human Golgi protein. The GP73 cDNA was cloned by differential screening of a cDNA library derived from the liver of a patient with adult giant-cell hepatitis (GCH), a rare form of hepatitis with presumed viral etiology. In vitro transcription–translation studies indicate that GP73 is an integral membrane protein, and immunolocalization experiments using epitope-tagged GP73 demonstrate that the protein is localized to the Golgi apparatus. Northern blot analysis of RNA from multiple human tissues reveals a single GP73 mRNA transcript with a size of approximately 3.0kb. Immunohistochemical studies using rabbit polyclonal antisera directed against recombinant GP73 demonstrate that the protein is preferentially expressed by epithelial cells in many human tissues. In normal livers, GP73 is consistently present in biliary epithelial cells, whereas hepatocytes show little or no signal. In contrast, livers of patients with GCH display strong GP73 immunoreactivity in multinucleated hepatocytes. GP73 mRNA and protein are expressed in highly differentiated HepG2 hepatoma cells after infection with adenovirus in vitro. We conclude that GP73 represents a novel, epithelial cell-specific integral membrane Golgi protein that can be upregulated in response to viral infection.
The Lancet | 1998
Andrew L. Mason; Lizhe Xu; Linsheng Guo; Santiago J. Munoz; Jonathan B. Jaspan; Michael Bryer-Ash; Yan Cao; David M. Sander; Yehuda Shoenfeld; Alaa Ahmed; Judy Van de Water; M. Eric Gershwin; Robert F. Garry
Summary Background Retroviruses have been implicated in the aetiology of various autoimmune diseases. We used immunoblots as a surrogate test to find out whether retroviruses play a part in the development of primary biliary cirrhosis. Methods We did western blot tests for HIV-1 and the human intracisternal A-type particle (HIAP), on serum samples from 77 patients with primary biliary cirrhosis, 126 patients with chronic liver disease, 48 patients with systemic lupus erythematosus, and 25 healthy volunteers. Findings HIV-1 p24 gag seroreactivity was found in 27 (35%) of 77 patients with primary biliary cirrhosis, 14 (29%) of 48 patients with systemic lupus erythematosus, 14 (50%) of 28 patients with chronic viral hepatitis, and nine (39%) of 23 patients with either primary sclerosing cholangitis or biliary atresia, compared with only one (4%) of 24 patients with alcohol-related liver disease or α 1 -antitrypsin-deficiency liver disease, and only one (4%) of 25 healthy volunteers (p=0·003). Western blot reactivity to more than two HIAP proteins was found in 37 (51%) of patients with primary biliary cirrhosis, in 28 (58%) of patients with systemic lupus erythematosus, in 15 (20%) of patients with chronic viral hepatitis, and in four (17%) of those with other biliary diseases. None of the 23 patients with either alcohol-related liver disease or α 1 -antitrypsin deficiency, and only one of the healthy controls showed the same reactivity to HIAP proteins (p Interpretation The HIV-1 and HIAP antibody reactivity found in patients with primary biliary cirrhosis and other biliary disorders may be attributable either to an autoimmune response to antigenically related cellular proteins or to an immune response to uncharacterised viral proteins that share antigenic determinants with these retroviruses.
The American Journal of Gastroenterology | 1998
Claus J. Fimmel; Linsheng Guo; Richard W. Compans; Elizabeth M. Brunt; Scot Hickman; Robert R. Perrillo; Andrew L. Mason
Adult syncytial giant cell hepatitis (GCH) is an uncommon and often fulminant form of hepatitis that may be caused by infection with a novel paramyxo-like virus. We present the case of a 69-yr-old man who presented with acute, community-acquired hepatitis and chronic lymphocytic leukemia. A liver biopsy showed the typical findings of panlobular syncytial giant cell hepatitis. Electron microscopic examination demonstrated abundant nucleocapsid-like protein material in the cytoplasm and nuclei of affected hepatocytes. These structures were similar to, but distinct from, those of known paramyxoviridae, suggesting infection with a novel, related virus. In situ hybridization studies with a probe directed against the measles fusion protein gene gave a positive signal with a hepatocyte distribution. No signal was obtained with the measles nucleocapsid protein probe, suggesting that the disease agent was genetically distinct from, but related to, the measles virus. Subsequent liver biopsies were characterized by the gradual disappearance of the giant cell changes and by the concomitant development of cirrhosis. This is a case of adult GCH that resolved spontaneously and led to cirrhosis, thus implicating GCH as a potential cause of “cryptogenic” liver disease. Our findings provide further support for the existence of a distinct, as yet unidentified viral species as a cause of this disease.
Clinical Transplantation | 2001
George E. Loss; Andrew L. Mason; Jamie Blazek; Debbie Dick; Jeane Lipscomb; Linsheng Guo; Robert P. Perrillo; James D. Eason
Here we describe a strategy for using livers from hepatitis B core antibody (anti‐HBc) positive donors in anti‐HBc negative recipients and report our preliminary results. Adult anti‐HBc negative recipients were immunized against hepatitis B virus (HBV) prior to transplantation. Liver biopsies from anti‐HBc positive, HBs Ag negative donors were performed at the time of procurement to rule out acute hepatitis or chronic liver disease. Donor serum and liver samples were collected for HBV DNA analysis by PCR.
Clinical Transplantation | 2007
Robert D Anderson; Srinath Chinnakotla; Linsheng Guo; Robert P. Perrillo; Goran B. Klintmalm; Gary L. Davis
Abstract: High titer hepatitis B immunoglobulin (HBIG) has significantly reduced the recurrence of hepatitis B virus (HBV) infection after liver transplantation. We compared our experience with intramuscular (IM) HBIG prophylaxis to our earlier outcomes with intravenous (IV) HBIG and other regimens.
Liver International | 2009
Lizhe Xu; Linsheng Guo; Zhiwei Shen; George E. Loss; Robert G. Gish; Shawn T. Wasilenko; Andrew L. Mason
Background: Primary biliary cirrhosis (PBC) is a complex disease with genetic and environmental influences. The disease is more prevalent in families with PBC and candidate gene case–control studies have linked PBC with DRB1*08 human leucocyte antigen class II alleles.
Hepatology | 1999
Andrew L. Mason; Joseph Lau; Nicole Hoang; Ke-Ping Qian; Graeme J. M. Alexander; Lizhe Xu; Linsheng Guo; Sheraj Jacob; Fredric G. Regenstein; Robert L. Zimmerman; James E. Everhart; Clive Wasserfall; Noel K. Maclaren; Robert P. Perrillo
Hepatology | 1998
Andrew L. Mason; Lizhe Xu; Linsheng Guo; Mary C. Kuhns; Robert P. Perrillo
Liver Transplantation | 2003
George E. Loss; Andrew L. Mason; Satheesh Nair; Jamie Blazek; Gist Farr; Linsheng Guo; Ari J. Cohen; James D. Eason