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1. Full Text Ex vivo analysis identifies effective HIV-1 latency-reversing drug combinations
by Laird, Gregory M and Bullen, C. Korin and Rosenbloom, Daniel I. S and Martin, Alyssa R and Hill, Alison L and Durand, Christine M and Siliciano, Janet D and Siliciano, Robert F
Journal of Clinical Investigation, ISSN 0021-9738, 05/2015, Volume 125, Issue 5, pp. 1901 - 1912
Reversal of HIV-1 latency by small molecules is a potential cure strategy. This approach will likely require effective drug combinations to achieve high levels... 
SUPPRESSIVE ANTIRETROVIRAL THERAPY | MEDICINE, RESEARCH & EXPERIMENTAL | VIRUS REACTIVATION | ACTIVATION | RESERVOIR | IN-VIVO | GENE-EXPRESSION | CD4(+) T-CELLS | HISTONE DEACETYLASE INHIBITORS | NF-KAPPA-B | LIFELONG PERSISTENCE | Anti-HIV Agents - pharmacology | Transcription, Genetic - drug effects | Lymphokines - secretion | Humans | Middle Aged | RNA, Messenger - analysis | Male | Virus Latency - drug effects | Anti-HIV Agents - administration & dosage | HIV-1 - physiology | Phorbol Esters - pharmacology | Adult | Anti-HIV Agents - therapeutic use | Female | CD4-Positive T-Lymphocytes - virology | Drug Evaluation, Preclinical | Bryostatins - pharmacology | HIV-1 - drug effects | Lymphocyte Activation | HIV Infections - virology | Protein Kinase C - drug effects | Cells, Cultured | RNA, Viral - analysis | Virion - metabolism | Azepines - pharmacology | Drug Synergism | Triazoles - pharmacology | CD4-Positive T-Lymphocytes - secretion | HIV Infections - drug therapy | Histone Deacetylase Inhibitors - pharmacology | Disulfiram - pharmacology | CD4-Positive T-Lymphocytes - drug effects | Physiological aspects | Research | RNA | T cells | Drug therapy | HIV infection | Studies | Statistical analysis | Cytokines | Acquired immune deficiency syndrome--AIDS | Lymphocytes | T cell receptors | Mathematical models | Gene expression | HIV | Infectious disease | AIDS
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2. Full Text FDA-approved selective estrogen receptor modulators inhibit ebola virus infection
by Johansen, Lisa M and Brannan, Jennifer M and Delos, Sue E and Shoemaker, Charles J and Stossel, Andrea and Lear, Calli and Hoffstrom, Benjamin G and DeWald, Lisa Evans and Schornberg, Kathryn L and Scully, Corinne and Lehár, Joseph and Hensley, Lisa E and White, Judith M and Olinger, Gene G
Science Translational Medicine, ISSN 1946-6234, 06/2013, Volume 5, Issue 190, pp. 190ra79 - 190ra79
Ebola viruses remain a substantial threat to both civilian and military populations as bioweapons, during sporadic outbreaks, and from the possibility of... 
MEDICINE, RESEARCH & EXPERIMENTAL | NIEMANN-PICK C1 | FILOVIRUS ENTRY | FUSION | HEMORRHAGIC FEVERS | HOST-CELL | ENDOTHELIAL-CELLS | MOUSE MODEL | IN-VIVO | GLYCOPROTEIN | BINDING | CELL BIOLOGY | Receptors, Estrogen - metabolism | United States | Humans | Cercopithecus aethiops | Drug Approval | Virus Internalization - drug effects | Endosomes - metabolism | Dose-Response Relationship, Drug | Ebolavirus - drug effects | Selective Estrogen Receptor Modulators - therapeutic use | Hemorrhagic Fever, Ebola - virology | Hydrogen-Ion Concentration - drug effects | Toremifene - therapeutic use | Endosomes - drug effects | Hemorrhagic Fever, Ebola - drug therapy | Vero Cells | Toremifene - pharmacology | United States Food and Drug Administration | Disease Models, Animal | Clomiphene - pharmacology | Mice, Inbred C57BL | Hep G2 Cells | Virion - drug effects | Clomiphene - therapeutic use | Animals | Cathepsins - metabolism | Survival Analysis | Mice | Ebolavirus - physiology | Selective Estrogen Receptor Modulators - pharmacology
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3. Full Text Suramin inhibits Zika virus replication by interfering with virus attachment and release of infectious particles
by Albulescu, Irina C and Kovacikova, Kristina and Tas, Ali and Snijder, Eric J and van Hemert, Martijn J
Antiviral Research, ISSN 0166-3542, 07/2017, Volume 143, pp. 230 - 236
Zika virus (ZIKV) is a mosquito-borne flavivirus that mostly causes asymptomatic infections or mild disease characterized by low-grade fever, rash,... 
DRUG | POTENT INHIBITOR | CHIKUNGUNYA | ENTRY | VIROLOGY | SCREEN | ENDOTHELIAL-CELLS | PHARMACOLOGY & PHARMACY | ENVELOPE PROTEIN | IDENTIFICATION | DENGUE VIRUS | BINDING | Mycophenolic Acid - antagonists & inhibitors | Zika Virus Infection - drug therapy | Cytopathogenic Effect, Viral - drug effects | DNA Replication - drug effects | Cercopithecus aethiops | Glycosylation - drug effects | Virus Internalization - drug effects | Suramin - administration & dosage | Suramin - antagonists & inhibitors | Zika Virus Infection - virology | Time Factors | Flavivirus - drug effects | Mycophenolic Acid - administration & dosage | Vero Cells | Virus Replication - drug effects | Zika Virus - growth & development | RNA, Viral - biosynthesis | Zika Virus - physiology | RNA, Viral - analysis | Zika Virus - drug effects | Virion - drug effects | Virus Attachment - drug effects | Virus Release - drug effects | Animals | RNA, Viral - drug effects | Birth defects | Conjunctivitis | Microbiology | RNA | Guillain-Barre syndrome
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4. Full Text Toremifene interacts with and destabilizes the Ebola virus glycoprotein
by Zhao, Yuguang and Ren, Jingshan and Harlos, Karl and Jones, Daniel M and Zeltina, Antra and Bowden, Thomas A and Padilla-Parra, Sergi and Fry, Elizabeth E and Stuart, David I
Nature, ISSN 0028-0836, 07/2016, Volume 535, Issue 7610, pp. 169 - 172
Ebola viruses (EBOVs) are responsible for repeated outbreaks of fatal infections, including the recent deadly epidemic in West Africa. There are currently no... 
SYSTEM | NIEMANN-PICK C1 | ENTRY | CHOLESTEROL | SMALL-MOLECULE INHIBITORS | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | ANTIBODY | RECEPTOR | INFECTION | HIV-1 VIRION FUSION | Temperature | Humans | Anti-Inflammatory Agents, Non-Steroidal - chemistry | Antiviral Agents - metabolism | Endosomes - metabolism | Protein Subunits - metabolism | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Ebolavirus - drug effects | Ibuprofen - chemistry | Antiviral Agents - chemistry | Endosomes - drug effects | Viral Envelope Proteins - metabolism | Conserved Sequence | Marburgvirus - chemistry | Anti-Inflammatory Agents, Non-Steroidal - metabolism | Binding Sites | Membrane Fusion - drug effects | Toremifene - metabolism | Toremifene - pharmacology | Cell Line | Antiviral Agents - pharmacology | Ibuprofen - pharmacology | Models, Molecular | Protein Structure, Quaternary - drug effects | Ibuprofen - metabolism | Virus Attachment - drug effects | Ebolavirus - chemistry | Viral Envelope Proteins - antagonists & inhibitors | Protein Stability - drug effects | Viral Envelope Proteins - chemistry | Hydrophobic and Hydrophilic Interactions | Protein Binding | Ligands | Protein Subunits - chemistry | Toremifene - chemistry | Ebola virus | Glycoproteins | Host-virus relationships | Observations | Health aspects | Drug interactions | Drug therapy | Binding sites | Viral infections | Crystal structure
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5. Full Text Modeling shows that the NS5A inhibitor daclatasvir has two modes of action and yields a shorter estimate of the hepatitis C virus half-life
by Jeremie Guedj and Harel Dahari and Libin Rong and Natasha D. Sansone and Richard E. Nettles and Scott J. Cotler and Thomas J. Layden and Susan L. Uprichard and Alan S. Perelson
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2013, Volume 110, Issue 10, pp. 3991 - 3996
The nonstructural 5A (NS5A) protein is a target for drug development against hepatitis C virus (HCV). Interestingly, the NS5A inhibitor daclatasvir... 
RNA | Virions | Antivirals | Viruses | Infections | Drug design | Kinetics | Dosage | Hepacivirus | Multiscale modeling | Viral dynamics | Direct-acting antiviral agents | Mathematical modeling | DOMAIN-III | LIVER-TRANSPLANTATION | direct-acting antiviral agents | PARTICLES | RNA REPLICATION | viral dynamics | MULTIDISCIPLINARY SCIENCES | ALPHA-INTERFERON | THERAPY | KINETICS | mathematical modeling | NONSTRUCTURAL PROTEIN | CELL-CULTURE | Hepacivirus - drug effects | Cell Line | Antiviral Agents - pharmacology | Humans | Middle Aged | Half-Life | Hepacivirus - genetics | Hepatitis C, Chronic - virology | Deoxycytidine - pharmacology | RNA, Viral - blood | Imidazoles - pharmacology | Hepatitis C, Chronic - drug therapy | RNA, Viral - genetics | Models, Biological | Bayes Theorem | Virus Assembly - drug effects | Adult | Female | Hepacivirus - physiology | Viral Load - drug effects | Viral Nonstructural Proteins - antagonists & inhibitors | Deoxycytidine - analogs & derivatives | Antiviral agents | Drug interactions | Physiological aspects | Dosage and administration | Research | Virulence (Microbiology) | Hepatitis C | Drug therapy | Biological Sciences | Physical Sciences
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6. Full Text SERINC3 and SERINC5 restrict HIV-1 infectivity and are counteracted by Nef
by Usami, Yoshiko and Wu, Yuanfei and Göttlinger, Heinrich G
Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7572, pp. 218 - 223
HIV-1 Nef and the unrelated mouse leukaemia virus glycosylated Gag (glycoGag) strongly enhance the infectivity of HIV-1 virions produced in certain cell types... 
CYTOPLASMIC DOMAIN | CELL-SURFACE CD4 | GLYCOSYLATED-GAG | VIRION FUSION | REPLICATION | PRIMARY T-LYMPHOCYTES | MULTIDISCIPLINARY SCIENCES | IMMUNODEFICIENCY-VIRUS TYPE-1 | CD4 DOWN-REGULATION | MURINE LEUKEMIA-VIRUS | OPTIMAL VIRAL INFECTIVITY | Humans | Neoplasm Proteins - antagonists & inhibitors | Neoplasm Proteins - pharmacology | Virion - chemistry | Host-Pathogen Interactions - drug effects | Membrane Proteins - pharmacology | Neoplasm Proteins - metabolism | Receptors, Cell Surface - antagonists & inhibitors | Membrane Proteins - deficiency | HIV-1 - growth & development | HIV-1 - physiology | HIV-1 - chemistry | Gene Deletion | nef Gene Products, Human Immunodeficiency Virus - metabolism | Membrane Proteins - metabolism | Cell Line | Virus Replication - drug effects | nef Gene Products, Human Immunodeficiency Virus - deficiency | HIV-1 - drug effects | Down-Regulation | HIV Infections - virology | Virion - physiology | CD4-Positive T-Lymphocytes - metabolism | Receptors, Cell Surface - metabolism | Gene Products, gag - metabolism | Protein Transport | Virion - drug effects | Membrane Proteins - antagonists & inhibitors | Receptors, Cell Surface - deficiency | HIV Infections - drug therapy | Neoplasm Proteins - deficiency | Virion - growth & development | Leukemia Virus, Murine - chemistry | Development and progression | Genetic aspects | Virulence (Microbiology) | Viral proteins | Properties | HIV infection | Proteins | Genomes | Immunology | Mutation | Human immunodeficiency virus--HIV | Cells
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7. Full Text Abrogated inflammatory response promotes neurogenesis in a murine model of Japanese encephalitis
by Das, Sulagna and Dutta, Kallol and Kumawat, Kanhaiya Lal and Ghoshal, Ayan and Adhya, Dwaipayan and Basu, Anirban
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 3, p. e17225
Background: Japanese encephalitis virus (JEV) induces neuroinflammation with typical features of viral encephalitis, including inflammatory cell infiltration,... 
PROGENITOR CELLS | NEURAL STEM-CELLS | SUBVENTRICULAR ZONE NEUROGENESIS | NEURONAL DEATH | FOCAL CEREBRAL-ISCHEMIA | BIOLOGY | NITRIC-OXIDE | ADULT HIPPOCAMPAL NEUROGENESIS | CENTRAL-NERVOUS-SYSTEM | NECROSIS-FACTOR-ALPHA | BLOOD-BRAIN-BARRIER | Solubility - drug effects | Encephalitis, Japanese - complications | Inflammation - pathology | Neurons - pathology | Encephalitis, Japanese - virology | Minocycline - pharmacology | Brain - virology | Cell Lineage - drug effects | Inflammation - complications | Inflammation Mediators - metabolism | Microglia - pathology | Neurogenesis - drug effects | Neurons - drug effects | Disease Models, Animal | Chemokines - biosynthesis | Microglia - drug effects | Neural Stem Cells - drug effects | Encephalitis Virus, Japanese - physiology | Virion - metabolism | Neural Stem Cells - pathology | Virion - drug effects | Brain - drug effects | Cell Movement - drug effects | Animals | Encephalitis, Japanese - pathology | Cell Differentiation - drug effects | Brain - pathology | Encephalitis Virus, Japanese - drug effects | Cell Proliferation - drug effects | Mice | Virus diseases | Inflammation | Research | Neurons | Analysis | Japanese encephalitis | Neuropathogenesis | Cell culture | Animal models | Leukemia | Memory | Viruses | Inflammatory response | Infections | Kinases | Neurogenesis | Cell activation | Cell growth | Epidermal growth factor | Neuroblasts | Rodents | Human immunodeficiency virus--HIV | Neurospheres | Minocycline | Degeneration | Trends | Conditioning | Vector-borne diseases | Encephalitis | Cytokines | Complications | Microglia | Brain research | Nitric oxide | Stem cells | Infiltration | Chemokines | Animal cognition | Side effects | neurospheres | Differentiation | HIV | Human immunodeficiency virus
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8. Full Text Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides
by Izquierdo-Useros, Nuria and Lorizate, Maier and Puertas, Maria C and Rodriguez-Plata, Maria T and Zangger, Nadine and Erikson, Elina and Pino, Maria and Erkizia, Itziar and Glass, Bärbel and Clotet, Bonaventura and Keppler, Oliver T and Telenti, Amalio and Kräusslich, Hans-Georg and Martinez-Picado, Javier
PLoS Biology, ISSN 1544-9173, 12/2012, Volume 10, Issue 12, p. e1001448
Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens. However, HIV-1 spread is strongly enhanced in... 
SIALOADHESIN | ACTIVATION | PARTICLES | DC-SIGN | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOLOGY | SUBSETS | HUMAN-IMMUNODEFICIENCY-VIRUS | MATURATION | CAPTURE | EXPRESSION | SUBCAPSULAR SINUS MACROPHAGES | Exosomes - drug effects | Exosomes - metabolism | Gene Silencing - drug effects | HIV Infections - virology | Humans | Virion - metabolism | Virion - drug effects | Up-Regulation - drug effects | HIV Infections - immunology | Immunological Synapses - drug effects | HIV-1 - physiology | HIV Infections - pathology | Gangliosides - metabolism | HEK293 Cells | Lipopolysaccharides - pharmacology | Sialic Acid Binding Ig-like Lectin 1 - metabolism | Dendritic Cells - drug effects | Liposomes - metabolism | Lipid Bilayers - metabolism | Dendritic Cells - virology | Dendritic Cells - metabolism | Studies | Acquired immune deficiency syndrome--AIDS | Microscopy | Pathogenesis | Lymphocytes | Rodents | Viruses | Experiments | Binding sites | Acquired immune deficiency syndrome | AIDS
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9. Full Text Luteolin restricts dengue virus replication through inhibition of the proprotein convertase furin
by Peng, Minhua and Watanabe, Satoru and Chan, Kitti Wing Ki and He, Qiuyan and Zhao, Ya and Zhang, Zhongde and Lai, Xiaoping and Luo, Dahai and Vasudevan, Subhash G and Li, Geng
Antiviral Research, ISSN 0166-3542, 07/2017, Volume 143, pp. 176 - 185
In many countries afflicted with dengue fever, traditional medicines are widely used as panaceas for illness, and here we describe the systematic evaluation of... 
Traditional Chinese medicine | Virus maturation | Furin | Antiviral therapy | Luteolin | Dengue virus | ACTIVATION | MECHANISM | VACCINE | MATURATION | ORGANIZATION | IN-VITRO | SEROTYPES | UNFOLDED PROTEIN RESPONSE | VIROLOGY | PHARMACOLOGY & PHARMACY | INFECTION | EXPRESSION | Dengue Virus - classification | DNA Replication - drug effects | Humans | Drugs, Chinese Herbal - pharmacology | Male | Dengue - drug therapy | Antiviral Agents - chemistry | Luteolin - chemistry | HEK293 Cells | Luteolin - administration & dosage | Proprotein Convertases - drug effects | Disease Models, Animal | Furin - metabolism | A549 Cells | Cell Line | Cell Survival - drug effects | Luteolin - antagonists & inhibitors | Virus Replication - drug effects | Antiviral Agents - pharmacology | Cricetinae | Dengue Virus - drug effects | Proprotein Convertases - metabolism | Dengue - virology | Viremia - drug therapy | Enzyme Activation - drug effects | Virion - drug effects | trans-Golgi Network - drug effects | Dengue Virus - genetics | Animals | Mice | Kinetics | RNA, Viral - drug effects | Virus diseases | Antiviral agents | Proteases | Analysis | Dengue viruses | Medicine, Chinese | Health aspects | Cells
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10. Full Text Modelling hepatitis C therapy-predicting effects of treatment
by Perelson, Alan S and Guedj, Jeremie and Los Alamos National Lab. (LANL), Los Alamos, NM (United States)
Nature Reviews Gastroenterology and Hepatology, ISSN 1759-5045, 08/2015, Volume 12, Issue 8, pp. 437 - 445
Mathematically modelling changes in HCV RNA levels measured in patients who receive antiviral therapy has yielded many insights into the pathogenesis and... 
VIRUS-RNA | GENOTYPE 1 | HCV NS5A INHIBITOR | SUPERINFECTION EXCLUSION | TRIPLE THERAPY | ANTIVIRAL ACTIVITY | CELL-LINES | GASTROENTEROLOGY & HEPATOLOGY | VIRAL KINETIC-MODEL | VIROLOGICAL RESPONSE | DYNAMICS IN-VIVO | Biomarkers - metabolism | Antiviral Agents - pharmacokinetics | Antiviral Agents - therapeutic use | Humans | Drug Resistance, Viral | Interferon-alpha - therapeutic use | Treatment Outcome | Hepatitis C, Chronic - drug therapy | Liver Regeneration - physiology | Viral Load | Virion - drug effects | Time Factors | Models, Biological | Interferon-alpha - pharmacokinetics | RNA, Viral - metabolism | Drug Therapy, Combination | RNA, Viral - drug effects | Antiviral agents | Complications and side effects | Dosage and administration | Research | Hepatitis C | Drug therapy | BASIC BIOLOGICAL SCIENCES | Biological Science
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11. Full Text The intracellular cholesterol transport inhibitor U18666A inhibits the exosome-dependent release of mature hepatitis C virus
by Elgner, Fabian and Ren, Huimei and Medvedev, Regina and Ploen, Daniela and Himmelsbach, Kiyoshi and Boller, Klaus and Hildt, Eberhard
Journal of Virology, ISSN 0022-538X, 2016, Volume 90, Issue 24, pp. 11181 - 11196
Hepatitis C virus (HCV) particles are described as lipoviroparticles which are released similarly to very-low-density lipoproteins (VLDLs). However, the... 
LIFE-CYCLE | ENDOSOMAL TRAFFICKING | PROTEIN | VIROLOGY | PARTICLES | RNA REPLICATION | CELL-CULTURE | INFECTION | AUTOPHAGY | VIRAL REPLICATION | APOLIPOPROTEIN-E | Exosomes - drug effects | Multivesicular Bodies - drug effects | Humans | Androstenes - pharmacology | Multivesicular Bodies - virology | Hepacivirus - physiology | Biological Transport - drug effects | Genes, Reporter | Hepatocytes - drug effects | Exosomes - ultrastructure | Exosomes - virology | Hepacivirus - drug effects | Gene Expression | Multivesicular Bodies - ultrastructure | Virion - physiology | Virus Assembly - physiology | Cholesterol - metabolism | Virion - drug effects | Virus Release - drug effects | Animals | Cell Line, Tumor | Hepatocytes - ultrastructure | Hepatocytes - virology | Virion - ultrastructure | Luminescent Proteins - genetics | Hepacivirus - ultrastructure | Anticholesteremic Agents - pharmacology | Luminescent Proteins - metabolism
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