Marcus J. Korth

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Integrated Omics Analysis of Pathogenic Host Responses during Pandemic H1N1 Influenza Virus Infection: The Crucial Role of Lipid Metabolism

Jennifer Tisoncik-Go, David J. Gasper, Jennifer E. Kyle, Amie J. Eisfeld, more

Cell Host & Microbe > 2016 > 19 > 2 > 254-266

Pandemic influenza viruses modulate proinflammatory responses that can lead to immunopathogenesis. We present an extensive and systematic profiling of lipids, metabolites, and proteins in respiratory compartments of ferrets infected with either 1918 or 2009 human pandemic H1N1 influenza viruses. Integrative analysis of high-throughput omics data with virologic and histopathologic data uncovered relationships...

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Drug repurposing: a better approach for infectious disease drug discovery?

G Lynn Law, Jennifer Tisoncik-Go, Marcus J Korth, Michael G Katze

Current Opinion in Immunology > 2013 > 25 > 5 > 588-592

The advent of publicly available databases containing system-wide phenotypic data of the host response to both drugs and pathogens, in conjunction with bioinformatics and computational methods now allows for in silico predictions of FDA-approved drugs as treatments against infection diseases. This systems biology approach captures the complexity of both the pathogen and drug host response in the form...

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Chronic immune activation is a distinguishing feature of liver and PBMC gene signatures from HCV/HIV coinfected patients and may contribute to hepatic fibrogenesis

Angela L. Rasmussen, I-Ming Wang, Margaret C. Shuhart, Sean C. Proll, more

Virology > 2012 > 430 > 1 > 43-52

Hepatitis C virus/human immunodeficiency virus (HCV/HIV) coinfected patients demonstrate accelerated progression to severe liver injury in comparison to HCV monoinfected patients, although the underlying mechanisms are unclear owing to infection of separate tissue compartments with two distinct viral pathogens. Microarray analysis of paired liver biopsy and peripheral blood mononuclear cell (PBMC)...

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Quantitative proteomic analysis of HIV-1 infected CD4+ T cells reveals an early host response in important biological pathways: Protein synthesis, cell proliferation, and T-cell activation

Arti T. Navare, Pavel Sova, David E. Purdy, Jeffrey M. Weiss, more

Virology > 2012 > 429 > 1 > 37-46

Human immunodeficiency virus (HIV-1) depends upon host-encoded proteins to facilitate its replication while at the same time inhibiting critical components of innate and/or intrinsic immune response pathways. To characterize the host cell response on protein levels in CD4+ lymphoblastoid SUP-T1 cells after infection with HIV-1 strain LAI, we used mass spectrometry (MS)-based global quantitation with...

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Early transcriptional programming links progression to hepatitis C virus–induced severe liver disease in transplant patients

Angela L. Rasmussen, Nicolas Tchitchek, Nathan J. Susnow, Alexei L. Krasnoselsky, more

Hepatology > 56 > 1 > 17 - 27

Liver failure resulting from chronic hepatitis C virus (HCV) infection is a major cause for liver transplantation worldwide. Recurrent infection of the graft is universal in HCV patients after transplant and results in a rapid progression to severe fibrosis and end‐stage liver disease in one third of all patients. No single clinical variable, or combination thereof, has, so far, proven accurate in...

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Virus–host interactions: from systems biology to translational research

Xinxia Peng, Eric Y Chan, Yu Li, Deborah L Diamond, more

Current Opinion in Microbiology > 2009 > 12 > 4 > 432-438

Research embracing systems biology approaches and careful analysis of the critical host response has greatly expanded our understanding of infectious diseases. First-generation studies based on genomics and proteomics have made significant progress in establishing the foundation for network-based investigations on virus–host interactions. More recently, data from complementary high-throughput technologies,...

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Decoding the multifaceted HIV-1 virus-host interactome

Eric Y Chan, Marcus J Korth, Michael G Katze

Journal of Biology > 2009 > 8 > 9 > 1-4

Recently in BMC Medical Genomics, Tozeren and colleagues have uncovered virus-host interactions by searching for conserved peptide motifs in HIV and human proteins. Their computational model provides a novel perspective in the interpretation of high-throughput data on the HIV-host interactome.

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Lost in the world of functional genomics, systems biology, and translational research: Is there life after the Milstein award?

Michael G. Katze, Marcus J. Korth

Cytokine and Growth Factor Reviews > 2007 > 18 > 5-6 > 441-450

We have always wanted to save the world from the scourges of virus infection by developing better drugs and vaccines. But fully understanding the intricacies of virus–host interactions, the first step in achieving this goal, requires the ability to view the process on a grand scale. The advent of high-throughput technologies, such as DNA microarrays and mass spectrometry, provided the first opportunities...

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Hijacking of the host-cell response and translational control during influenza virus infection

John C. Kash, Alan G. Goodman, Marcus J. Korth, Michael G. Katze

Virus Research > 2006 > 119 > 1 > 111-120

Influenza virus is a major public health problem with annual deaths in the US of 36,000 with pandemic outbreaks, such as in 1918, resulting in deaths exceeding 20 million worldwide. Recently, there is much concern over the introduction of highly pathogenic avian influenza H5N1 viruses into the human population. Influenza virus has evolved complex translational control strategies that utilize cap-dependent...

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Functional gene analysis of individual response to challenge of SIVmac239 in M. mulatta PBMC culture

Matthew J. Thomas, Michael B. Agy, Sean C. Proll, Bryan W. Paeper, more

Virology > 2006 > 348 > 1 > 242-252

It has previously been shown in macaques that individual animals exhibit varying responses to challenge with the same strain of SIV. We attempted to elucidate these differences using functional genomics and correlate them to biological response. Unfractionated PBMC from three rhesus macaques were isolated, activated, and infected with SIVmac239. Interestingly, one of the three animals used for these...

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Gene Expression Patterns That Correlate With Hepatitis C and Early Progression to Fibrosis in Liver Transplant Recipients

Maria W. Smith, Kathie–Anne Walters, Marcus J. Korth, Matthew Fitzgibbon, more

Gastroenterology > 2006 > 130 > 1 > 179-187

Background & Aims: Liver transplant recipients infected with hepatitis C virus (HCV) develop recurrent hepatitis soon after transplantation and, in some cases, progress to fibrosis within the first 2 years. Our goals were to identify molecular processes influencing the liver disease progression and to find potential gene markers of early fibrosis. Methods: We performed gene expression profiling...

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Hepatitis C virus and liver disease: Global transcriptional profiling and identification of potential markers

Maria W. Smith, Zhaoxia N. Yue, Marcus J. Korth, Hao A. Do, more

Hepatology > 2003 > 38 > 6 > 1458-1467

Microarray analysis of RNA from hepatitis C virus (HCV)-infected cirrhotic livers was performed to identify a gene expression signature of liver disease. The expression levels of approximately 13,600 genes were analyzed using surgical material and core biopsy specimens from HCV-infected cirrhotic liver explants in comparison with reference samples of normal nondiseased liver. In addition, normal liver...

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P52 ^r ^IPK Regulates the Molecular Cochaperone P58 ^IPK To Mediate Control of the RNA-Dependent Protein Kinase in Response to Cytoplasmic Stress ^†

Michael Gale,, Collin M. Blakely, André Darveau, Patrick R. Romano, more

Biochemistry > 2002 > 41 > 39 > 11878 - 11887

article

Interferon Inhibits the Replication of HIV-1, SIV, and SHIV Chimeric Viruses by Distinct Mechanisms

Marcus J. Korth, Matthew D. Taylor, Michael G. Katze

Virology > 1998 > 247 > 2 > 265-273

Interferon (IFN) treatment of lentivirus-infected cells substantially reduces virus replicationin vitro. Although the replication of both HIV-1 and simian immunodeficiency virus (SIV) is inhibited, IFN blocks the replication of these viruses at different stages of the viral life cycle. We previously demonstrated that in HIV-1–infected cells, IFN blocks a late step in viral replication, leading to...

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Repression of the PKR protein kinase by the hepatitis C virus NS5A protein: a potential mechanism of interferon resistance

Michael J. Gale, Jr., Marcus J. Korth, Michael G. Katze

Clinical and Diagnostic Virology > 1998 > 10 > 2-3 > 157-162

Background: Chronic infection with hepatitis C virus (HCV) is associated with progressive liver damage, including the development of cirrhosis and hepatocellular carcinoma, and HCV is a leading cause of liver dysfunction worldwide. The current therapy for chronic HCV infection, interferon-α (IFN), is effective in a minority of HCV-infected patients. Several studies have demonstrated a correlation...

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Interferon Treatment Inhibits the Replication of Simian Immunodeficiency Virus at an Early Stage: Evidence for a Block between Attachment and Reverse Transcription

Matthew D. Taylor, Marcus J. Korth, Michael G. Katze

Virology > 1998 > 241 > 1 > 156-162

Interferon (IFN) dramatically reduces both SIV and HIV-1 replicationin vitro. However, we previously found that whereas IFN treatment of SIV-infected cells results in a decrease in the level of viral RNA, IFN treatment of HIV-1-infected cells has no effect on viral RNA expression but rather leads to a decrease in viral protein stability and a deregulation of polyprotein processing (M. B. Agy, R. L...

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Evidence That Hepatitis C Virus Resistance to Interferon Is Mediated through Repression of the PKR Protein Kinase by the Nonstructural 5A Protein

Michael J. Gale, Marcus J. Korth, Norina M. Tang, Seng-Lai Tan, more

Virology > 1997 > 230 > 2 > 217-227

Hepatitis C virus (HCV) is the major cause of non-A non-B hepatitis and a leading cause of liver dysfunction worldwide. While the current therapy for chronic HCV infection is parenteral administration of type 1 interferon (IFN), only a fraction of HCV-infected individuals completely respond to treatment. Previous studies have correlated the IFN sensitivity of strain HCV-1b with mutations within a...

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Cloning, expression, and cellular localization of the oncogenic 58-kDa inhibitor of the RNA-activated human and mouse protein kinase

Marcus J. Korth, Christopher N. Lyons, Marlene Wambach, Michael G. Katze

Gene > 1996 > 170 > 2 > 181-188

The 58-kDa inhibitor of the interferon-induced double-stranded RNA-activated protein kinase (PKR) is a cellular protein that is activated during influenza virus infection to down-regulate the activity of PKR. This study was initiated to further our understanding of the inhibitor which, when overproduced, has the capacity to malignantly transform cells. We report here the isolation and characterization...

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Chromosomal Assignment of the Gene Encoding the Human 58-kDa Inhibitor (PRKRI) of the Interferon-Induced dsRNA-Activated Protein Kinase to Chromosome 13q32

Marcus J. Korth, Susanne Edelhoff, Christine M. Disteche, Michael G. Katze

Genomics > 1996 > 31 > 2 > 238-239

The 58-kDa inhibitor (p58) of the interferon-induced dsRNA-activated protein kinase (PKR) is a cellular protein recruited by the influenza virus to down-regulate the activity of PKR during virus infection. The inhibitor also appears to play a role in the regulation of cellular gene expression in the absence of viral infection and has oncogenic properties when overexpressed. Using fluorescencein situhybridization,...

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Search results for: Marcus J. Korth

Integrated Omics Analysis of Pathogenic Host Responses during Pandemic H1N1 Influenza Virus Infection: The Crucial Role of Lipid Metabolism

Drug repurposing: a better approach for infectious disease drug discovery?

Chronic immune activation is a distinguishing feature of liver and PBMC gene signatures from HCV/HIV coinfected patients and may contribute to hepatic fibrogenesis

Quantitative proteomic analysis of HIV-1 infected CD4+ T cells reveals an early host response in important biological pathways: Protein synthesis, cell proliferation, and T-cell activation

Early transcriptional programming links progression to hepatitis C virus–induced severe liver disease in transplant patients

Virus–host interactions: from systems biology to translational research

Decoding the multifaceted HIV-1 virus-host interactome

Lost in the world of functional genomics, systems biology, and translational research: Is there life after the Milstein award?

Hijacking of the host-cell response and translational control during influenza virus infection

Functional gene analysis of individual response to challenge of SIVmac239 in M. mulatta PBMC culture

Gene Expression Patterns That Correlate With Hepatitis C and Early Progression to Fibrosis in Liver Transplant Recipients

Hepatitis C virus and liver disease: Global transcriptional profiling and identification of potential markers

P52 ^r ^IPK Regulates the Molecular Cochaperone P58 ^IPK To Mediate Control of the RNA-Dependent Protein Kinase in Response to Cytoplasmic Stress ^†

Interferon Inhibits the Replication of HIV-1, SIV, and SHIV Chimeric Viruses by Distinct Mechanisms

Repression of the PKR protein kinase by the hepatitis C virus NS5A protein: a potential mechanism of interferon resistance

Interferon Treatment Inhibits the Replication of Simian Immunodeficiency Virus at an Early Stage: Evidence for a Block between Attachment and Reverse Transcription

Evidence That Hepatitis C Virus Resistance to Interferon Is Mediated through Repression of the PKR Protein Kinase by the Nonstructural 5A Protein

Cloning, expression, and cellular localization of the oncogenic 58-kDa inhibitor of the RNA-activated human and mouse protein kinase

Chromosomal Assignment of the Gene Encoding the Human 58-kDa Inhibitor (PRKRI) of the Interferon-Induced dsRNA-Activated Protein Kinase to Chromosome 13q32

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