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  • 1
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    Efficient initiation of HCV RNA replication in cell culture (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-09
    Description: Hepatitis C virus (HCV) infection is a global health problem affecting an estimated 170 million individuals worldwide. We report the identification of multiple independent adaptive mutations that cluster in the HCV nonstructural protein NS5A and confer increased replicative ability in vitro. Among these adaptive mutations were a single amino acid substitution that allowed HCV RNA replication in 10% of transfected hepatoma cells and a deletion of 47 amino acids encompassing the interferon (IFN) sensitivity determining region (ISDR). Independent of the ISDR, IFN-alpha rapidly inhibited HCV RNA replication in vitro. This work establishes a robust, cell-based system for genetic and functional analyses of HCV replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blight, K J -- Kolykhalov, A A -- Rice, C M -- AI40034/AI/NIAID NIH HHS/ -- CA57973/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1972-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110-1093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11110665" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Hepacivirus/drug effects/genetics/*physiology ; Humans ; Interferon-alpha/pharmacology ; Mutation ; Phosphorylation ; Point Mutation ; RNA Replicase/genetics/metabolism ; RNA, Viral/*biosynthesis ; *Replicon ; Sequence Deletion ; Transfection ; Tumor Cells, Cultured ; Viral Nonstructural Proteins/*genetics/*metabolism ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Transmission of hepatitis C by intrahepatic inoculation with transcribed RNA (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: More than 1% of the world's population is chronically infected with hepatitis C virus (HCV). HCV infection can result in acute hepatitis, chronic hepatitis, and cirrhosis, which is strongly associated with development of hepatocellular carcinoma. Genetic studies of HCV replication have been hampered by lack of a bona fide infectious molecular clone. Full-length functional clones of HCV complementary DNA were constructed. RNA transcripts from the clones were found to be infectious and to cause disease in chimpanzees after direct intrahepatic inoculation. This work defines the structure of a functional HCV genome RNA and proves that HCV alone is sufficient to cause disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolykhalov, A A -- Agapov, E V -- Blight, K J -- Mihalik, K -- Feinstone, S M -- Rice, C M -- AI40034/AI/NIAID NIH HHS/ -- CA57973/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):570-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110-1093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; Consensus Sequence ; DNA, Complementary ; Hepacivirus/*genetics/physiology ; Hepatitis C/*transmission/*virology ; Liver/*virology ; Molecular Sequence Data ; Pan troglodytes ; Polymerase Chain Reaction ; RNA, Messenger/*genetics ; RNA, Viral/blood/*genetics ; Transfection ; Viremia ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Sindbis virus: an efficient, broad host range vector for gene expression in animal cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-03-03
    Description: Sindbis virus, an enveloped virus with a single-stranded RNA genome, was engineered to express a bacterial protein, chloramphenicol acetyltransferase (CAT), in cultured insect, avian, and mammalian cells. The vectors were self-replicating and gene expression was efficient and rapid; up to 10(8) CAT polypeptides were produced per infected cell in 16 to 20 hours. CAT expression could be made temperature-sensitive by means of a derivative that incorporated a temperature-sensitive mutation in viral RNA synthesis. Vector genomic RNAs were packaged into infectious particles when Sindbis helper virus was used to supply virion structural proteins. The vector RNAs were stable to at least seven cycles of infection. The expression of CAT increased about 10(3)-fold, despite a 10(15)-fold dilution during the passaging. Sindbis virus vectors should prove useful for expressing large quantities of gene products in a variety of animal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiong, C -- Levis, R -- Shen, P -- Schlesinger, S -- Rice, C M -- Huang, H V -- AG05681/AG/NIA NIH HHS/ -- AI11377/AI/NIAID NIH HHS/ -- AI24134/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1188-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2922607" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes ; Animals ; Bacteria/enzymology ; Cells, Cultured ; Chick Embryo ; Chloramphenicol O-Acetyltransferase/*genetics ; Codon ; Cricetinae ; DNA/genetics ; Drosophila ; Gene Amplification ; Gene Expression Regulation ; *Genetic Engineering ; *Genetic Vectors ; Humans ; Quail ; RNA, Viral/*genetics ; Sindbis Virus/*genetics ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Virology. Getting rid of a persistent troublemaker to cure hepatitis (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shlomai, Amir -- Rice, Charles M -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1212-3. doi: 10.1126/science.1252186.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiviral Agents/*pharmacology ; DNA, Circular/*metabolism ; DNA, Viral/*metabolism ; Hepatitis B/*drug therapy ; Hepatitis B virus/*drug effects ; Hepatocytes/*drug effects ; Humans ; Interferon-alpha/*pharmacology ; Lymphotoxin beta Receptor/*agonists
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    HCV persistence and immune evasion in the absence of memory T cell help (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: Spontaneous resolution of hepatitis C virus (HCV) infection in humans usually affords long-term immunity to persistent viremia and associated liver diseases. Here, we report that memory CD4+ Tcells are essential for this protection. Antibody-mediated depletion of CD4+ Tcells before reinfection of two immune chimpanzees resulted in persistent, low-level viremia despite functional intra-hepatic memory CD8+ Tcell responses. Incomplete control of HCV replication by memory CD8+ Tcells in the absence of adequate CD4+ Tcell help was associated with emergence of viral escape mutations in class I major histocompatibility complex-restricted epitopes and failure to resolve HCV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grakoui, Arash -- Shoukry, Naglaa H -- Woollard, David J -- Han, Jin-Hwan -- Hanson, Holly L -- Ghrayeb, John -- Murthy, Krishna K -- Rice, Charles M -- Walker, Christopher M -- A14736/PHS HHS/ -- AI40034/AI/NIAID NIH HHS/ -- AI48231/AI/NIAID NIH HHS/ -- CA57973/CA/NCI NIH HHS/ -- CA85883/CA/NCI NIH HHS/ -- N01 HB27091/HB/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Hepatitis C, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576438" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antigen Presentation ; Antigens, Viral/chemistry/genetics/immunology ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Epitopes ; Evolution, Molecular ; Hepacivirus/genetics/*immunology/*physiology ; Hepatitis C/*immunology/virology ; *Immunologic Memory ; Liver/immunology ; Major Histocompatibility Complex ; Molecular Sequence Data ; Mutation ; Pan troglodytes ; T-Lymphocyte Subsets/immunology ; Time Factors ; Viral Core Proteins/chemistry/genetics/immunology ; Viral Nonstructural Proteins/chemistry/genetics/immunology ; Viremia ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Complete replication of hepatitis C virus in cell culture (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-11
    Description: Many aspects of the hepatitis C virus (HCV) life cycle have not been reproduced in cell culture, which has slowed research progress on this important human pathogen. Here, we describe a full-length HCV genome that replicates and produces virus particles that are infectious in cell culture (HCVcc). Replication of HCVcc was robust, producing nearly 10(5) infectious units per milliliter within 48 hours. Virus particles were filterable and neutralized with a monoclonal antibody against the viral glycoprotein E2. Viral entry was dependent on cellular expression of a putative HCV receptor, CD81. HCVcc replication was inhibited by interferon-alpha and by several HCV-specific antiviral compounds, suggesting that this in vitro system will aid in the search for improved antivirals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lindenbach, Brett D -- Evans, Matthew J -- Syder, Andrew J -- Wolk, Benno -- Tellinghuisen, Timothy L -- Liu, Christopher C -- Maruyama, Toshiaki -- Hynes, Richard O -- Burton, Dennis R -- McKeating, Jane A -- Rice, Charles M -- AI40034/AI/NIAID NIH HHS/ -- AI50798/AI/NIAID NIH HHS/ -- AI51820/AI/NIAID NIH HHS/ -- CA10702/CA/NCI NIH HHS/ -- CA57973/CA/NCI NIH HHS/ -- CA85883/CA/NCI NIH HHS/ -- DK70497/DK/NIDDK NIH HHS/ -- G0400802/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2005 Jul 22;309(5734):623-6. Epub 2005 Jun 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15947137" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antibodies, Viral/immunology ; Antigens, CD/metabolism ; Antigens, CD81 ; Antiviral Agents/pharmacology ; Cell Line, Tumor ; Centrifugation, Density Gradient ; Culture Media, Conditioned ; Genome, Viral ; Hepacivirus/genetics/immunology/*physiology ; Humans ; Interferon-alpha/pharmacology ; Mutation ; Neutralization Tests ; RNA, Viral/biosynthesis ; Replicon ; Serial Passage ; Transfection ; Viral Envelope Proteins/analysis/biosynthesis ; Viral Nonstructural Proteins/analysis/biosynthesis ; Virion/physiology ; *Virus Cultivation ; *Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Mycobacterial disease and impaired IFN-gamma immunity in humans with inherited ISG15 deficiency (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-04
    Description: ISG15 is an interferon (IFN)-alpha/beta-inducible, ubiquitin-like intracellular protein. Its conjugation to various proteins (ISGylation) contributes to antiviral immunity in mice. Here, we describe human patients with inherited ISG15 deficiency and mycobacterial, but not viral, diseases. The lack of intracellular ISG15 production and protein ISGylation was not associated with cellular susceptibility to any viruses that we tested, consistent with the lack of viral diseases in these patients. By contrast, the lack of mycobacterium-induced ISG15 secretion by leukocytes-granulocyte, in particular-reduced the production of IFN-gamma by lymphocytes, including natural killer cells, probably accounting for the enhanced susceptibility to mycobacterial disease. This experiment of nature shows that human ISGylation is largely redundant for antiviral immunity, but that ISG15 plays an essential role as an IFN-gamma-inducing secreted molecule for optimal antimycobacterial immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507439/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507439/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bogunovic, Dusan -- Byun, Minji -- Durfee, Larissa A -- Abhyankar, Avinash -- Sanal, Ozden -- Mansouri, Davood -- Salem, Sandra -- Radovanovic, Irena -- Grant, Audrey V -- Adimi, Parisa -- Mansouri, Nahal -- Okada, Satoshi -- Bryant, Vanessa L -- Kong, Xiao-Fei -- Kreins, Alexandra -- Velez, Marcela Moncada -- Boisson, Bertrand -- Khalilzadeh, Soheila -- Ozcelik, Ugur -- Darazam, Ilad Alavi -- Schoggins, John W -- Rice, Charles M -- Al-Muhsen, Saleh -- Behr, Marcel -- Vogt, Guillaume -- Puel, Anne -- Bustamante, Jacinta -- Gros, Philippe -- Huibregtse, Jon M -- Abel, Laurent -- Boisson-Dupuis, Stephanie -- Casanova, Jean-Laurent -- 1R37AI095983-01/AI/NIAID NIH HHS/ -- 5R01AI035237-15/AI/NIAID NIH HHS/ -- 8UL1TR000043/TR/NCATS NIH HHS/ -- AI096090/AI/NIAID NIH HHS/ -- CA072943/CA/NCI NIH HHS/ -- R01 AI035237/AI/NIAID NIH HHS/ -- R01 AI091707/AI/NIAID NIH HHS/ -- R01 AI096090/AI/NIAID NIH HHS/ -- R01 CA072943/CA/NCI NIH HHS/ -- R37 AI095983/AI/NIAID NIH HHS/ -- UL1 TR000043/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1684-8. Epub 2012 Aug 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22859821" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/blood ; Cytokines/genetics/*immunology ; Female ; Granulocytes/immunology ; Humans ; Immunity ; Interferon-gamma/*immunology ; Interleukin-12/immunology ; Killer Cells, Natural/immunology ; Male ; Mice ; Mycobacterium Infections/blood/genetics/*immunology ; Pedigree ; T-Lymphocytes/immunology ; Ubiquitins/genetics/*immunology ; Virus Diseases/blood/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Nucleotide sequence of yellow fever virus: implications for flavivirus gene expression and evolution (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-23
    Description: The sequence of the entire RNA genome of the type flavivirus, yellow fever virus, has been obtained. Inspection of this sequence reveals a single long open reading frame of 10,233 nucleotides, which could encode a polypeptide of 3411 amino acids. The structural proteins are found within the amino-terminal 780 residues of this polyprotein; the remainder of the open reading frame consists of nonstructural viral polypeptides. This genome organization implies that mature viral proteins are produced by posttranslational cleavage of a polyprotein precursor and has implications for flavivirus RNA replication and for the evolutionary relation of this virus family to other RNA viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, C M -- Lenches, E M -- Eddy, S R -- Shin, S J -- Sheets, R L -- Strauss, J H -- AI 10793/AI/NIAID NIH HHS/ -- AI 20612/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 23;229(4715):726-33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4023707" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Biological Evolution ; Gene Expression Regulation ; Genes ; Glycoproteins/genetics ; Nucleic Acid Conformation ; Protein Biosynthesis ; Protein Conformation ; Protein Processing, Post-Translational ; RNA, Viral/*genetics ; Viral Proteins/*genetics ; *Virus Replication ; Yellow fever virus/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Mouse models of acute and chronic hepacivirus infection (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-07-14
    Description: An estimated 71 million people worldwide are infected with hepatitis C virus (HCV). The lack of small-animal models has impeded studies of antiviral immune mechanisms. Here we show that an HCV-related hepacivirus discovered in Norway rats can establish high-titer hepatotropic infections in laboratory mice with immunological features resembling those seen in human viral hepatitis. Whereas immune-compromised mice developed persistent infection, immune-competent mice cleared the virus within 3 to 5 weeks. Acute clearance was T cell dependent and associated with liver injury. Transient depletion of CD4 + T cells before infection resulted in chronic infection, characterized by high levels of intrahepatic regulatory T cells and expression of inhibitory molecules on intrahepatic CD8 + T cells. Natural killer cells controlled early infection but were not essential for viral clearance. This model may provide mechanistic insights into hepatic antiviral immunity, a prerequisite for the development of HCV vaccines.
    Keywords: Immunology, Microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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